Cancer - Associated Thrombosis - A Study of Cases.

Research shows that the presence of cancer increases the likelihood of developing venous thromboembolism (pulmonary thromboembolism and deep vein thrombosis) from as much as fourfold up to sevenfold. It is imperative that after early diagnosis we treat cancer-associated thrombosis with grave seriousness in order to reduce its morbidity and mortality. We present 14 case reports of patients with cancer-associated thrombosis including thrombosis related to malignant hemopathies.

Special Conditions in Venous Thrombembolism - Case Series.

Venous thromboembolism (VTE), including deep vein thrombosis (DVT) and pulmonary embolism (PE), is a preventable cause of in-hospital death, and one of the most prevalent vascular diseases. There is a lack of knowledge with regards to contemporary presentation, management, and outcomes of patients with VTE. Many clinically important subgroups (including the elderly, those with recent bleeding, renal insufficiency, disseminated malignancy or pregnant patients) have been under-represented in randomized clinical trials.

FC gamma receptor polymorphisms in patients with immune thrombocytopenia.

Introduction: Immune thrombocytopenia (ITP) is an autoimmune blood disease of unknown etiology. The aim of our study was to investigate a possible role of FCGR2A and FCGR3A polymorphisms in the development of primary ITP.

Methods: We analyzed 125 adult patients with ITP and 120 healthy controls.

Molecular Response in Patients with Chronic Myeloid Leukemia Treated with Imatinib - Single Centre Experience.

Introduction of tyrosine kinase inhibitors (TKI) dramatically improves the treatment and survival of the patients with chronic myeloid leukemia (CML) in the last decade. Imatinib (IM) and other TKI induce larger percentage of complete cytogenetic response (CCyR) and major molecular response (MMR). Treatment resistance to TKIs still remains an important problem in the treatment of CML.

CTLA-4 exon 1 polymorphism in patients with autoimmune blood disorders.

CTLA-4 is a CD28 homologue that plays an important role in negative regulation of T-cell responses. Its transient expression on the surface of activated T cells antagonizes the activating signals and terminates the T-cell response. An A to G polymorphism at position 49 of the CTLA-4 first exon has recently been associated with several autoimmune disorders.