Heparin-induced thrombocytopenia risk factors: Difference between revisions
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* There is no increase in risk of HIT with genetic risk factors for thrombosis such as [[factor V Leiden]], [[prothrombin]] gene mutation, [[methylenetetrahydrofolate reductase]] ([[MTHFR]]) polymorphism and platelet-receptor polymorphisms. | * There is no increase in risk of HIT with genetic risk factors for thrombosis such as [[factor V Leiden]], [[prothrombin]] gene mutation, [[methylenetetrahydrofolate reductase]] ([[MTHFR]]) polymorphism and platelet-receptor polymorphisms. | ||
* Polymorphisms in the [[crystallized fragment]] (Fc) gamma receptor have been suggested to play in role in the risk for HIT. It is presumed that high affinity receptors result in stronger IgG binding to platelet membranes, allowing for the release of procoagulants. | * Polymorphisms in the [[crystallized fragment]] (Fc) gamma receptor have been suggested to play in role in the risk for HIT. It is presumed that high affinity receptors result in stronger IgG binding to platelet membranes, allowing for the release of procoagulants. | ||
* PF4 optical density (OD): The degree of elevation of the OD valve of the PF4 IgG is directly correlated with the risk for HIT. For patients with a Pf4 IgG OD of < 0.4, the risk of HIT is typically < 5%. No follow up testing is required. For patients with a PF4 IgG OD of 1 | * PF4 optical density (OD): The degree of elevation of the OD valve of the PF4 IgG is directly correlated with the risk for HIT. For patients with a Pf4 IgG OD of < 0.4, the risk of HIT is typically < 5%. No follow up testing is required. For patients with a PF4 IgG OD of > 1.0, the risk of HIT is signicantly higher (3.4-6-fold increase risk of thrombosis), requiring follow up testing with a functional assay such as the 14C-serotonin release assay or the heparin-induced platelet aggregation assay.<ref name="pmid20059332">{{cite journal| author=Arepally GM, Ortel TL| title=Heparin-induced thrombocytopenia. | journal=Annu Rev Med | year= 2010 | volume= 61 | issue= | pages= 77-90 | pmid=20059332 | doi=10.1146/annurev.med.042808.171814 | pmc=4153429 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20059332 }} </ref> | ||
'''Protective''' risk factors include: | '''Protective''' risk factors include: | ||
Revision as of 21:37, 9 July 2017
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Heparin-induced thrombocytopenia |
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Differentiating Heparin-induced thrombocytopenia from other Diseases |
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Diagnosis |
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Heparin-induced thrombocytopenia risk factors On the Web |
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Directions to Hospitals Treating Heparin-induced thrombocytopenia |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2], Aric C. Hall, M.D., [3] Shyam Patel [4]
Overview
Heparin-induced thrombocytopenia is diagnosed when the platelet count falls by > 50% typically after 5-10 days of heparin therapy. Increased risks for heparin-induced thrombocytopenia depends on type of heparin (unfractionated heparin > low molecular weight heparin), duration of therapy, females and type of patients (commoner in surgical patients that require large amount of heparin)
Risk factors
Adverse risk factors include:[1]
- Duration of heparin treatment: A long duration of heparin expsosure, such as 2 weeks, is associated with the greatest risk.
- Type of heparin: Unfractionated heparin (UFH) has a greater risk than low molecular weight heparin (LMWH. Bovine heparin carries a higher risk for HIT than porcine heparin.[2]
- Type of patient: Surgical patients are at higher risk than medical; cardiac surgical patients have the highest risk of all.[3] This is though to be related to differences in basal level of circulating platelet factor 4 (PF4) and platelet activation in these various populations. The incidence of HIT in cardiac surgery or orthopedic surgery patients is 1-5%.[4]
- Sex: Females have a higher risk than males. The odds ratio (OR) is 2.4:1.[3] This is thought to be related to higher predilection for autoimmune tendencies in females compared to males.
- Race: African Americans are more prone to HIT than Caucasians.[3]
- There is no increase in risk of HIT with genetic risk factors for thrombosis such as factor V Leiden, prothrombin gene mutation, methylenetetrahydrofolate reductase (MTHFR) polymorphism and platelet-receptor polymorphisms.
- Polymorphisms in the crystallized fragment (Fc) gamma receptor have been suggested to play in role in the risk for HIT. It is presumed that high affinity receptors result in stronger IgG binding to platelet membranes, allowing for the release of procoagulants.
- PF4 optical density (OD): The degree of elevation of the OD valve of the PF4 IgG is directly correlated with the risk for HIT. For patients with a Pf4 IgG OD of < 0.4, the risk of HIT is typically < 5%. No follow up testing is required. For patients with a PF4 IgG OD of > 1.0, the risk of HIT is signicantly higher (3.4-6-fold increase risk of thrombosis), requiring follow up testing with a functional assay such as the 14C-serotonin release assay or the heparin-induced platelet aggregation assay.[2]
Protective risk factors include:
- Type of warfarin: Use of low molecular weight heparin such as enoxaparin carries a lower risk for HIT. Porcine heparin carries a lower risk for HIT compared to bovine heparin.[2]
- Type of patient: Pediatric or obstetric patients have a lower risk for HIT than medical or surgical patients. Obstetrics patients have a 0.1-1% risk of developing HIT, as compared to 1-5% risk in surgical patients.[4]
- PF4 optical density: A low PF4 IgG OD of less than 0.4 suggests a very low risk for HIT.
Reference
- ↑ Warkentin TE, Sheppard JA, Sigouin CS, Kohlmann T, Eichler P, Greinacher A. Gender imbalance and risk factor interactions in heparin-induced thrombocytopenia. Blood 2006;108:2937-41. PMID 16857993.
- ↑ 2.0 2.1 2.2 Arepally GM, Ortel TL (2010). "Heparin-induced thrombocytopenia". Annu Rev Med. 61: 77–90. doi:10.1146/annurev.med.042808.171814. PMC 4153429. PMID 20059332.
- ↑ 3.0 3.1 3.2 Lee GM, Arepally GM (2013). "Diagnosis and management of heparin-induced thrombocytopenia". Hematol Oncol Clin North Am. 27 (3): 541–63. doi:10.1016/j.hoc.2013.02.001. PMC 3668315. PMID 23714311.
- ↑ 4.0 4.1 Linkins LA, Dans AL, Moores LK, Bona R, Davidson BL, Schulman S; et al. (2012). "Treatment and prevention of heparin-induced thrombocytopenia: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines". Chest. 141 (2 Suppl): e495S–e530S. doi:10.1378/chest.11-2303. PMC 3278058. PMID 22315270.