000			03087nam a22003617a 4500
008			221213s20222022 xxu||||| |||| 00| 0 eng d
022			_a2000-9666
024			_a10.55729/2000-9666.1102 [doi]
024			_ajchim-12-05-102 [pii]
024			_aPMC9529653 [pmc]
040			_aOvid MEDLINE(R)
099			_a36262487
245			_aA Case Report and Literature Review on Argatroban Refractory Heparin-Induced Thrombocytopenia.
251			_aJournal of Community Hospital Internal Medicine Perspectives. 12(5):102-105, 2022.
252			_aJ Community Hosp Intern Med Perspect. 12(5):102-105, 2022.
253			_aJournal of community hospital internal medicine perspectives
260			_c2022
260			_fFY2023
265			_sepublish
266			_d2022-12-13
520			_aHeparin-induced thrombocytopenia (HIT) is characterized by low platelets and thrombosis after exposure to Heparin products. It is classically characterized by a rapid and significant drop in platelets and life-threatening thrombosis. Thrombosis can occur up to 50% of the cases if left untreated. It requires immediate discontinuation of all heparin products and switching to a non-heparin anticoagulant to prevent further thrombosis. Here we present a case of a 56-year-old male who presented to the Emergency Department with sudden onset of severe left leg pain. Duplex study showed arterial thrombosis in the common iliac and distal iliac arteries. He received TPA at once and underwent thrombectomy while his platelet continued to drop. He used Low Molecular Weight Heparin (enoxaparin) for bridging after his tonsil surgery a week prior to this hospital admission. His HIT assay was found to be positive and despite the Argatroban therapy his clinical condition continued to worsen while his platelet count continued to drop. Given the refractory nature of the thrombosis and thrombocytopenia; Intravenous immunoglobulin (IVIG) therapy was introduced. The patient showed a great response and his platelet count improved to 150,000/mu. He was discharged on warfarin with a closer follow-up. Few case reports have described the treatment of such refractory cases using intravenous immunoglobulin (IVIG), resulting in stabilized platelet counts, reduced platelet activation, and reduced thrombotic complications, the exact mechanism of which is unknown. It is thought that IVIG inhibits platelet activation by binding as platelet receptors, which would otherwise bind with heparin-platelet factor 4 complexes and HIT antibodies. Copyright © 2022 Greater Baltimore Medical Center.
546			_aEnglish
650			_aIN PROCESS -- NOT YET INDEXED
651			_aMedStar Union Memorial Hospital
656			_aInternal Medicine Residency
657			_aCase Reports
700			_aDeen, Imad U _bMUMH _cInternal Medicine Residency _dMBBS _eResident PGY 3
700			_aJha, Swati A _bMUMH
700			_aMustafa, Sadaf _bMUMH
790			_aDeen IU, Jha SA, Mustafa S
856			_uhttps://dx.doi.org/10.55729/2000-9666.1102 _zhttps://dx.doi.org/10.55729/2000-9666.1102
942			_cART _dArticle
999			_c78 _d78