A. Kandoria, S. Rao, P. Negi, R. Bhardwaj, K. Mahajan, N. Gaur
{"title":"肝素诱导的血小板减少症:一个基于病例的重新评估","authors":"A. Kandoria, S. Rao, P. Negi, R. Bhardwaj, K. Mahajan, N. Gaur","doi":"10.15761/ccsr.1000120","DOIUrl":null,"url":null,"abstract":"Heparin‐induced thrombocytopenia (HIT) is an immune mediated adverse drug reaction caused by the emergence of antibodies that activate platelets in the presence of heparin. Despite thrombocytopenia, bleeding is rare. HIT is strongly associated with thromboembolic complications involving both the arterial and venous systems. A number of laboratory tests are available to confirm the diagnosis; however, when HIT is clinically suspected, treatment should not be withheld pending the result. Fortunately, therapeutic strategies have been refined, and new and effective therapeutic agents are available. We present a case of HIT Type II. A review of HIT is presented, examining the important clinical symptoms and diagnostic indicators. The treatment of HIT is then discussed, with an emphasis on current therapies. An extensive literature review has been performed to present a comprehensive review of the causes, pathophysiology and treatment of HIT. *Correspondence to: Somendra Rao, MD Senior Resident, Department of Cardiology Indira Gandhi Medical College, Shimla, India, E-mail: sureshdev. rao@gmail.com Received: March 07, 2019; Accepted: March 26, 2019; Published: March 28, 2019 Introduction There are two types of HIT described. Type I is a non-immune, mediated, asymptomatic, transient drop in platelet count that occurs in some heparin treated patients. It is typically characterized by a lesser fall in platelet count within the first two days after heparin initiation and often returns to normal with continued heparin administration [1,2]. Type II (HIT-II) is an immune-mediated disorder characterized by the formation of antibodies against heparin-platelet factor 4 complexes. Since The frequency of HIT varies from 0.5% to 5%, depending on the patient population studied [3]. A meta-analysis noted an incidence of 2.6 percent [4]. It has recently been proposed that the term “HIT type I” be changed to “non‐immune heparin associated thrombocytopenia” and that the term “HIT type II” be changed to “HIT” to avoid confusion between the two syndromes","PeriodicalId":10345,"journal":{"name":"Clinical Case Studies and Reports","volume":"24 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Heparin induced thrombocytopenia: A case-based re-appraisal\",\"authors\":\"A. Kandoria, S. Rao, P. Negi, R. Bhardwaj, K. Mahajan, N. Gaur\",\"doi\":\"10.15761/ccsr.1000120\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Heparin‐induced thrombocytopenia (HIT) is an immune mediated adverse drug reaction caused by the emergence of antibodies that activate platelets in the presence of heparin. Despite thrombocytopenia, bleeding is rare. HIT is strongly associated with thromboembolic complications involving both the arterial and venous systems. A number of laboratory tests are available to confirm the diagnosis; however, when HIT is clinically suspected, treatment should not be withheld pending the result. Fortunately, therapeutic strategies have been refined, and new and effective therapeutic agents are available. We present a case of HIT Type II. A review of HIT is presented, examining the important clinical symptoms and diagnostic indicators. The treatment of HIT is then discussed, with an emphasis on current therapies. An extensive literature review has been performed to present a comprehensive review of the causes, pathophysiology and treatment of HIT. *Correspondence to: Somendra Rao, MD Senior Resident, Department of Cardiology Indira Gandhi Medical College, Shimla, India, E-mail: sureshdev. rao@gmail.com Received: March 07, 2019; Accepted: March 26, 2019; Published: March 28, 2019 Introduction There are two types of HIT described. Type I is a non-immune, mediated, asymptomatic, transient drop in platelet count that occurs in some heparin treated patients. It is typically characterized by a lesser fall in platelet count within the first two days after heparin initiation and often returns to normal with continued heparin administration [1,2]. Type II (HIT-II) is an immune-mediated disorder characterized by the formation of antibodies against heparin-platelet factor 4 complexes. Since The frequency of HIT varies from 0.5% to 5%, depending on the patient population studied [3]. A meta-analysis noted an incidence of 2.6 percent [4]. It has recently been proposed that the term “HIT type I” be changed to “non‐immune heparin associated thrombocytopenia” and that the term “HIT type II” be changed to “HIT” to avoid confusion between the two syndromes\",\"PeriodicalId\":10345,\"journal\":{\"name\":\"Clinical Case Studies and Reports\",\"volume\":\"24 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Clinical Case Studies and Reports\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.15761/ccsr.1000120\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical Case Studies and Reports","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.15761/ccsr.1000120","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Heparin induced thrombocytopenia: A case-based re-appraisal
Heparin‐induced thrombocytopenia (HIT) is an immune mediated adverse drug reaction caused by the emergence of antibodies that activate platelets in the presence of heparin. Despite thrombocytopenia, bleeding is rare. HIT is strongly associated with thromboembolic complications involving both the arterial and venous systems. A number of laboratory tests are available to confirm the diagnosis; however, when HIT is clinically suspected, treatment should not be withheld pending the result. Fortunately, therapeutic strategies have been refined, and new and effective therapeutic agents are available. We present a case of HIT Type II. A review of HIT is presented, examining the important clinical symptoms and diagnostic indicators. The treatment of HIT is then discussed, with an emphasis on current therapies. An extensive literature review has been performed to present a comprehensive review of the causes, pathophysiology and treatment of HIT. *Correspondence to: Somendra Rao, MD Senior Resident, Department of Cardiology Indira Gandhi Medical College, Shimla, India, E-mail: sureshdev. rao@gmail.com Received: March 07, 2019; Accepted: March 26, 2019; Published: March 28, 2019 Introduction There are two types of HIT described. Type I is a non-immune, mediated, asymptomatic, transient drop in platelet count that occurs in some heparin treated patients. It is typically characterized by a lesser fall in platelet count within the first two days after heparin initiation and often returns to normal with continued heparin administration [1,2]. Type II (HIT-II) is an immune-mediated disorder characterized by the formation of antibodies against heparin-platelet factor 4 complexes. Since The frequency of HIT varies from 0.5% to 5%, depending on the patient population studied [3]. A meta-analysis noted an incidence of 2.6 percent [4]. It has recently been proposed that the term “HIT type I” be changed to “non‐immune heparin associated thrombocytopenia” and that the term “HIT type II” be changed to “HIT” to avoid confusion between the two syndromes