Differential Diagnosis: Secondary ITP
There is no substantial difference in immunologic pathophysiology between primary and secondary immune thrombocytopenia (ITP): it is characterized by increased platelet destruction in the reticuloendothelial system or reduced platelet production mediated
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bstract There is no substantial difference in immunologic pathophysiology between primary and secondary immune thrombocytopenia (ITP): it is characterized by increased platelet destruction in the reticuloendothelial system or reduced platelet production mediated primarily by IgG antiplatelet autoantibodies, resulting in thrombocytopenia. Secondary ITP can occur in the context of a variety of underlying diseases or conditions, including autoimmune diseases, such as systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS), lymphoproliferative disorders, and chronic infection with certain bacterial or viral microorganisms, including Helicobacter pylori (H. pylori), hepatitis C virus (HCV), and human immunodeficiency virus (HIV). Therefore, patients diagnosed as having ITP should be further evaluated for symptoms, physical signs, and laboratory tests associated with underlying disorders that potentially cause secondary ITP. It is imperative to consider risk factors in an individual patient basis. For example, elderly in H. pylori epidemic countries, such as East Asia and Italy, should be considered for performing H. pylori testing, homosexuals and drug abusers for performing HIV and HCV testing, and young women with a rash, fever, or arthralgia for performing a series of autoantibody tests. In clinical practice, identification of underlying diseases or conditions is essential in patients diagnosed as having ITP since treatment strategies are often different between primary and secondary ITP.
T. Satoh (*) Division of Hematology, Kitasato University School of Allied Health Sciences, 1-15-1 Kitasato, Minami-ku, Sagamihara, Kanagawa 252-0373, Japan Division of Molecular Hematology, Kitasato University Graduate School of Medical Sciences, 1-15-1 Kitasato, Minami, Sagamihara, Kanagawa 252-0374, Japan e-mail: [email protected] M. Kuwana Department of Allergy and Rheumatology, Nippon Medical School Graduate School of Medicine, 1-1-5 Sendagi, Bunkyo-ku, Tokyo 113-8603, Japan e-mail: [email protected] © Springer Nature Singapore Pte Ltd. 2017 Y. Ishida, Y. Tomiyama (eds.), Autoimmune Thrombocytopenia, DOI 10.1007/978-981-10-4142-6_9
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T. Satoh and M. Kuwana
1 Introduction Based on the proposal by an international working group organized for the standardization of definitions and classifications for immune thrombocytopenia (ITP), ITP can be divided into two forms [1]. ITP can occur in the absence of an apparent predisposing etiology (primary ITP) or as a sequela of an associated condition (secondary ITP). There is no substantial difference in immunologic pathophysiology between primary and secondary ITP: it is characterized by increased platelet destruction in the reticuloendothelial system or reduced platelet production primarily mediated by antiplatelet autoantibodies to platelet surface glycoproteins (GPs), resulting in thrombocytopenia [2]. Nevertheless, distinction of primary and secondary ITP is a major challenge in clinical setting, because they often require different treatment algorithm. N
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