ABSTRACT
This short review gives a brief overview on recent findings about the roles of basophils and mast cells in acquired and innate immunity. We try to give some insight into the methods used to study physiologic functions of mast cells and basophils. We mention variations of circulating basophil numbers as an epiphenomenon of some internal diseases and present an update on mastocytosis.
Subject(s)
Basophils/immunology , Basophils/pathology , Hematologic Diseases/immunology , Hematologic Diseases/pathology , Mast Cells/immunology , Mastocytosis/immunology , Mastocytosis/pathology , Animals , Clinical Trials as Topic , Humans , Mast Cells/pathologyABSTRACT
As there is no single, simple and reliable laboratory method to test the entire hemostasis the evaluation of patients with hemorrhagic complications remains a multistep process. A detailed history and clinical examination is central in the planning and interpretation of laboratory tests. The present work emphasizes on history taking and guides general practitioners in choosing and interpreting appropriate screening tests.
Subject(s)
Hemorrhage/diagnosis , Adult , Blood Coagulation Disorders/diagnosis , Blood Coagulation Tests , Female , Hemorrhage/chemically induced , Hemorrhage/etiology , Hemorrhage/genetics , Hemorrhagic Disorders/diagnosis , Hemostasis , Humans , Male , Physical Examination , Time FactorsABSTRACT
Recurrent thromboembolism despite oral anticoagulation is primarily suspicious of overt or occult neoplasia. We report on a man (age: 67 years) who presented with severe thrombophilia which was only controlled when the patient was set on a combined anticoagulation with low molecular weight heparin in supratherapeutic dosage and phenprocoumon with a target INR of 2.0. Despite repeated evaluation over about two years, a malignant tumour could never be demonstrated. However, the patient suffered in addition to a protein S deficiency from an antiphosphospholipid syndrome and a chronic myelomonocytic leukaemia. We postulate that the accepted strong thrombogenicity of antiphosphospholipid syndrome was further increased by protein S deficiency and a possibly procoagulatory effect of the abnormal monocytes explaining the severe thrombophilia resistant to standard therapeutic anticoagulation with a vitamin K antagonist and usual therapeutic doses of low molecular weight heparin, respectively.
Subject(s)
Anticoagulants/therapeutic use , Pulmonary Embolism/diagnostic imaging , Thrombosis/chemically induced , Aged , Antiphospholipid Syndrome/blood , Antiphospholipid Syndrome/diagnostic imaging , Blood Coagulation Tests , Heparin, Low-Molecular-Weight/therapeutic use , Humans , Male , Phenprocoumon/therapeutic use , Pulmonary Embolism/blood , Pulmonary Embolism/drug therapy , Recurrence , Thrombosis/blood , Thrombosis/diagnostic imaging , Tomography, X-Ray ComputedABSTRACT
The migration of neutrophil leukocytes to inflammatory sites is important for the elimination of microorganisms but can under pathological conditions lead to severe tissue damage. The initial chemotactic response is elicited by classical chemoattractants, such as fMet-Leu-Phe or the chemokine interleukin-8 which ligate to G-protein coupled receptors. Neutrophils show also a delayed chemotactic response to growth factors, such as platelet derived growth factor (PDGF) or tumor growth factor (TGF beta). We describe here that classical chemoattractants and growth factors stimulate neutrophil chemotaxis through different signal transduction pathways. Wortmannin, a selective phosphatidylinositol 3-kinase inhibitor, completely blocks growth factor stimulated chemotaxis while having no effect on neutrophil migration stimulated with classical chemoattractants. The results suggest that cell migration can be selectively controlled through the inhibition of distinct signal transduction events.
