Interrelation between light and ultrastructure study of bone marrow in thrombocytopenic patients with chronic liver diseases: morphological changes and factors affecting thrombopoiesis

Abstract number: CD071

Helmy^* A., Abdel Aziz^* I., Adel† D., Abdel Rahman^* Y.

†Matarya Hospital, Egypt ^*Theodor Bilhars RI Research ReT.B.R.I, Egypt;

Thrombopoietein (Tpo) is the major cytokine involved in the growth and development of megakaryocytes and the regulation of platelets production. Thrombopoietein serum level depends on hepatic Tpo production and platelets turn over. Erythropoietein, IL11, and stem cell factor can synergisize with Tpo in the support of megakaryocyte colony growth. This work was conducted to clarify the contribution of platelets production, consumption, coagulation, morphology and splenic sequestration to thrombocytopenia in chronic liver diseases. Platelets count, PT, serum Tpo, erythropoietein, d-dimers, PF4 were performed in 30 patients with liver disease (child stage A, B, C), 10 patients for each stage. Bone marrow aspiration from 15 patients of them, five patients for each stage (after their consent) were examined by light and electron microscopy for any morphological changes. Spleen size was estimated by computer tomography. Cases of child stage A revealed normal PT, Tpo serum level, PF4, d-dimers, erythropoietein level and no morphological abnormalities. In child stage B, C Tpo and erythropoietein showed significant decreased level as compared to normal whereas PT, PF4 and, d-dimers were of normal level. Micromegkaryocytes and defect in platelets budding were observed by light microscopy. Electron microscopic examination of megakaryocytes revealed degeneration, dilatation of demarcation membrane, decrease in alpha granules and endoplasmic reticulum, deficient cytoskeleton formation and immature granules were disclosed. Ultrastructural examination of platelets showed variations in size & shape as decreased granulation, distended mitochondria and increased giant platelets. From this study we concluded that the mechanism of thrombocytopenia associated with reduced hepatic Tpo in advanced liver diseases can be attributed not only to the decreased production of megakaryocytes but also to the abnormally formed and degenerated megakaryocytes with subsequent variation in size and shape of platelets which are liable to be destroyed as highlighted by electron microscopy study.

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