Glycemic dysregulation in a patient with type 2 diabetes treated with 5-azacitidine: a case report.

Background: Diabetes and myelodysplastic syndrome are two conditions that may coexist in a single patient, since both diseases are prevalent in the elderly. The pathophysiology of myelodysplastic syndrome involves recurrent genetic mutations, especially in genes controlling epigenetic regulation. Although the pathophysiology of diabetes is not well understood, several studies suggest a role of epigenetics in type 2 diabetes.

A CASE OF CHORIORETINOPATHY AS FIRST MANIFESTATION OF HODGKIN'S LYMPHOMA.

Purpose: To report a case of chorioretinopathy, which preceded diagnosis of Hodgkin's lymphoma.

Methods: Single patient case report.

Results: A 61-year-old woman with a history of breast cancer in remission and low-grade follicular lymphoma without criteria of high tumor burden presented with bilateral multifocal chorioretinopathy.

Unexpected low prevalence of atrial fibrillation in cryptogenic ischemic stroke: a prospective study.

Purpose: Ischemic stroke is a frequent pathology with high rate of recurrence and significant morbidity and mortality. There are several causes of stroke, affecting prognosis, outcomes, and management, but in many cases, the etiology remains undetermined. We hypothesized that atrial fibrillation was involved in this pathology but underdiagnosed by standard methods.

Effectiveness of a new immunoassay for the diagnosis of heparin-induced thrombocytopenia and improved specificity when detecting IgG antibodies.

The diagnosis of heparin-induced thrombocytopenia (HIT) is based on clinical criteria and biological assays. Most immunoassays detect antibodies (either IgG alone or additionally IgA and IgM) against PF4 immobilised in wells of microtiter plates with stoichiometric concentrations of polyanion (heparin or polyvinylsulfonate). We studied whether diagnostic sensitivity and/or specificity for HIT could be improved using a novel assay in which unfractionated heparin is immobilised alone to the microwells, with PF4 (and, potentially, other heparin-dependent antigen proteins) provided by adding platelet lysate during the procedure.

Increased tissue factor expression is associated with reduced survival in non-small cell lung cancer and with mutations of TP53 and PTEN.

Background: Tissue factor (TF), the main initiator of blood coagulation, is also a signaling protein that regulates cancer progression. TF synthesis was recently shown to be affected by tumor suppressor genes (TSGs) in tumor cell lines. We therefore studied TF gene (F3) expression and the status of genes coding for tumor protein p53 (TP53), phosphatase and tensin homolog (PTEN), and serine/threonine kinase 11 (STK11) in non-small cell lung cancer (NSCLC).

The intracellular localization of ID2 expression has a predictive value in non small cell lung cancer.

Background: ID2 is a member of a subclass of transcription regulators belonging to the general bHLH (basic-helix-loop-helix) family of transcription factors. In normal cells, ID2 is responsible for regulating the balance between proliferation and differentiation. More recent studies have demonstrated that ID2 is involved in tumor progression in several cancer types such as prostate or breast.

Usefulness of pretest clinical score (4Ts) combined with immunoassay for the diagnosis of heparin-induced thrombocytopenia.

Purpose Of Review: This review addresses the clinical and biological strategy to be applied for the diagnosis of heparin-induced thrombocytopenia.

Recent Findings: Heparin-induced thrombocytopenia is a severe prothrombotic disease caused by immunoglobulin G antibodies, which bind to platelet factor 4 and activate platelets with subsequent increased thrombin generation. Venous and arterial thromboses are frequent, explaining why substituting heparin with a potent alternative anticoagulant (danaparoid, lepirudin, or argatroban) is necessary in every affected patient.

Tissue factor expression in non-small cell lung cancer: relationship with vascular endothelial growth factor expression, microvascular density, and K-ras mutation.

Introduction: Tissue factor (TF) is the physiological trigger of blood coagulation, but it could also have an important role in cancer by regulating VEGF expression and angiogenesis.

Methods: TF expression was studied by real-time PCR in lung tumors of 64 patients with non-small-cell lung cancer (NSCLC) and by immunohistochemical analysis. The gene expression of two VEGF isoforms, VEGF165 and VEGF189, was also evaluated.

Fibrinogen Aalpha-Thr312Ala and factor XIII-A Val34Leu polymorphisms in idiopathic venous thromboembolism.

Introduction: Fibrinogen Aalpha-Thr312Ala and Factor XIII Val34Leu polymorphisms have been shown to modify fibrin clot structure and function. However, clinical studies have yielded conflicting results on their possible association with venous thromboembolism (VTE).

Methods: We studied the association between these two polymorphisms and VTE in a hospital-based case-control study.

Influence of MMP-2 and MMP-9 promoter polymorphisms on gene expression and clinical outcome of non-small cell lung cancer.

Matrix metalloproteinases (MMP) including MMP-2 and MMP-9 play a major role in tumour invasion by proteolysing the extracellular matrix. Their activation, particularly that of MMP-9, is partly dependent on plasmin that is inhibited by TFPI-2 (tissue factor pathway inhibitor-2), a serine protease inhibitor whose gene expression is decreased in about one-third of non-small cell lung cancers (NSCLC). In addition, MMP-2 and MMP-9 are essential in the development of NSCLC and can be regulated by functional promoter polymorphisms.

Expression of the human kallikrein genes 10 (KLK10) and 11 (KLK11) in cancerous and non-cancerous lung tissues.

Only one transcript for KLK10 was identified by RT-PCR in lung tissue, whereas KLK11 expressed at least four alternative transcripts. Quantitative analysis of KLK10 and KLK11 expression levels was assessed by real-time PCR, in a cohort of 47 patients with non-small-cell lung cancer (NSCLC). Expression levels of these genes were widely distributed in the population studied.

[Heparin-induced thrombocytopenia].

Heparin-induced thrombocytopenia (HIT) is due to IgG antibodies specific to platelet factor 4. HIT is characterized by a delayed decrease in platelet count (after the 5th day of treatment) often associated with thromboses. The presence of heparin-dependent antibodies has to be demonstrated to confirm HIT by ELISA or platelet activation tests.

Molecular bases of antithrombin deficiency: twenty-two novel mutations in the antithrombin gene.

Antithrombin (AT) is a major physiological inhibitor of hemostasis. We report 22 novel antithrombin gene (SERPINC1) mutations associated with antithrombin deficiency in 17 French and five German families. They were all present at the heterozygous state.

Increased prevalence of factor V Leiden in patients with retinal vein occlusion and under 60 years of age.

Retinal vein occlusion (RVO) is a multifactorial disease involving vessel damage, stasis, viscosity and thrombosis. Conflicting findings on hereditary thrombophilic risk factors have been reported and their impact on RVO features remains to be defined. The aim of the present study was to evaluate the prevalence of hereditary thrombophilic risk factors (HTRF) and characteristics of RVO in patients with or without HTRF.

Changes in platelet count after cardiac surgery can effectively predict the development of pathogenic heparin-dependent antibodies.

Cardiopulmonary bypass (CPB) induces the release of platelet factor 4 (PF4) and patients are at risk of heparin-induced thrombocytopenia (HIT). This study was aimed to determine whether an abnormal evolution in platelet count (PC) after CPB is predictive of the development of HIT antibodies. Two abnormal PC patterns were defined: pattern P1, characterized by a decrease in PC following previous correction of thrombocytopenia occurring during CPB, and pattern P2, defined as a persistent low PC in the days following CPB.

Ischaemic strokes and homozygosity for the alpha2 807T allele of the platelet collagen receptor in young monozygotic twins.

A nucleotide 807T variant of the glycoprotein Ia gene that correlates with increased platelet surface levels of the platelet collagen receptor alpha2beta1 was recently found to be associated with an increased risk of ischaemic stroke in younger patients. We report the history of twins who developed ischaemic strokes and were shown to be homozygous for the alpha2 807T allele. The twins developed ischaemic strokes at the ages of 23 and 33 years, one of them with recurrent events.