Evaluación de los factores determinantes del recuento de plaquetas en pacientes con cirrosis

Thrombocytopenia is considered one of the hallmarks of patients with cirrhosis. Several mechanisms have been implicated in the pathophysiology of thrombocytopenia in cirrhosis. Hypersplenism caused by splenomegay, classically regarded as an indirect marker of portal hypertension has been considered the main factor implicated [200]. Nevertheless, portal hypertension is best estimated by the hepatic venous pressure gradient (HVPG) [32, 189], although contradictory results have been reported regarding the association between HVPG and platelet count [195-197]. The identification of thrombopoietin (TPO), a growth factor that enhances the maturation of megakaryocytes and the release of platelets from the bone marrow, has shed new light on the physiolgy of platelets [217]. In normal conditions in adults, TPO is mainly produced in the liver [93, 96] and the circulating leves of platelets are controlled by a negative feedback mechanism [99], so there is an inverse relationship between the amount of circulating platelets, and the amount of TPO that can reach the bone marrow to stimulate thrombopoiesis. In liver cirrhosis perhaps a decreased syntehesis of TPO could be implicated in the development of thrombocytopenia. Controversial findings regarding the role of each mechanism in thrombocytopenia of liver cirrhosis have been reported [142, 146, 160-161, 184] and no study has simultaneously evaluated the influence of the different mechanisms including portal hypertension and TPO production nor whether their influence could change in different stages of the disease..

Additional file 1: Table S2. of Novel roles of DC-SIGNR in colon cancer cell adhesion, migration, invasion, and liver metastasis

The table shows the clinical data of the colon cancer patients in DC-SIGNR ELISA study. (DOCX 24 kb

Additional file 4: Figure S1. of Novel roles of DC-SIGNR in colon cancer cell adhesion, migration, invasion, and liver metastasis

DC-SIGNR did not promote colony formation in colon cancer cells. (A) The photographs indicated no influence of DC-SIGNR protein on cell proliferation efficiency of LoVo cells. (B) The histograms showed the clone cells number in respective cells. (TIF 1926 kb