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Platelet Aggregation, Platelet Serotonin and Pancreatitis

Fuad Lechin*, Bertha van der Dijs

Department of Physiological Sciences, Instituto de Medicina Experimental, Universidad Central de Venezuela. Caracas, Venezuela

*Corresponding Author:
Fuad Lechin
Apartado 80.983
Caracas 1080-A
Tel +58.212.961.1048
Fax +58.212.961.0172
E-mail [email protected]

Received: May 26th, 2004

Visit for more related articles at JOP. Journal of the Pancreas


Pancreatitis; Platelet Adhesiveness; Platelet Aggregation; Serotonin; Thrombosis


beta-TG: betathromboglobulin; f-5HT: plasma serotonin; ITP: idiopathic thrombocytopenic purpura; PF4: platelet factor 4; p-5HT: platelet-serotonin

Dear Sir:

The article by Mimidis et al. [1] prompted us to contribute some additional information. The authors studied acute pancreatitis patients showing increased platelet adhesiveness and aggregation. They postulate that the platelet activation factor is the most important mediator involved in the process and triggers platelet activation. They also discuss the mechanisms played by the membrane integrin glycoprotein IIb/IIIa. Furthermore, they made reference to membrane receptors for fibrinogen and the calcium-dependent linkage formation between activated receptors and bivalent fibrinogen which results in platelet aggregation. They also referred to proaggregatory mediators such as ADP, ATP, platelet factor 4 (PF4), betathromboglobulin (beta-TG), thromoboxane A2 (TXA2), fibrinogen and thrombospondin which are followed by the translocation of alpha-granule membrane protein P-selectin (CD62). Finally, they mentioned the role played by phosphatidylserine which is the starting point for the coagulation cascade. They also referred to the alterations of the platelet function described in models of systemic inflammation such as ulcerative colitis, Crohn's disease and acute pancreatitis.

With respect to all of the above, we would like to further elucidate the role played by platelet-serotonin (p-5HT) in thrombogenesis. This factor, rather than the platelet count, seems to constitute the true index of thrombogenesis [2, 3]. With respect to the above, we successfully treated five cases of refractory idiopathic thrombocytopenic purpura (ITP) using a neuropharmacological therapy aimed at enhancing (central nervous system) noradrenergic activity. Surprisingly, restoration of p-5HT levels, rather than the platelet count, was correlated with bleeding stoppage and clinical improvement. The above findings are consistent with the fact that serotonin is stored in the delta granules of platelets.

The release of serotonin is considered to be the "gold standard" assay for the detection of thrombocyte activation [4]. The presence of serotonin is covalently linked to fibrinogen bound on the surface of the activated platelet where it increases the retention of procoagulant factors on the cell surface [5]. Serotonin, therefore, occupies a central role in the hamostatic process, and its release is considered the most reliable assay for platelet activation [4].

Our findings are in line with those obtained by Dominguez et al. [6] who showed a lack of correlation between the platelet count and bleeding in an experimental model of immune thrombocytopenic purpura in mice. The fact that not only acute pancreatitis [7, 8] but other inflammatory diseases, such as ulcerative colitis [9, 10] and Crohn's disease [11, 12, 13], showed similar platelet disorders is consistent with findings which show that these diseases present with increased platelet aggregability secondary to the elevated circulating adrenaline which is always present. The latter phenomenon is responsible both for the reduction of p-5HT and the increase of plasma serotonin (f-5HT). Thus, we believe that the fundamental role played by platelet serotonin in thrombogenesis should not have been omitted in the discussion of the article by Mimidis et al. [1].


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