The role of heparin-associated antiplatelet antibodies in the outcome of arterial reconstruction

Calaitges, John; Liem, Timothy K.; Spadone, Donald P.; Nichols, W. Kirt; Silver, Donald

doi:10.1016/s0741-5214(99)70203-x

Cited by 34 publications

(19 citation statements)

References 26 publications

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“…In addition to mediating HIT, heparin-PF4 antibodies are independent predictors of adverse outcomes in various patient populations, particularly cardiac and cardiovascular surgery patients [5][6][7][8][9][10][11][12], and some experts suggest including heparin-PF4 antibodies in the preoperative cardiac surgery risk profile [9]. We observed in medical, neurotrauma, or shock-trauma ICU patients that the median durations of ICU stay and hospital stay were greater in seropositive patients than seronegative patients, which is suggestive of a possible effect, yet few thrombotic or fatal events occurred overall.…”

Section: Discussionmentioning

confidence: 99%

“…The recommended treatment for HIT is to stop heparin immediately and initiate fast-acting, nonheparin anticoagulation [3,4]. Even in the absence of thrombocytopenia, heparin-PF4 antibody seropositivity is associated with increased thrombotic risk, length of hospitalization, or mortality in cardiac [5,6], cardiovascular surgery [7][8][9], orthopedic surgery [10], hemodialysis [11], and pediatric intensive care unit (ICU) patients [12]. Antibody-associated endothelial cell activation may play a role in the pathophysiology of these effects [13].…”

Section: Introductionmentioning

confidence: 99%

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Heparin–platelet factor 4 antibodies in intensive care patients: an observational seroprevalence study

Levine

Hergenroeder²,

Francis

et al. 2009

J Thromb Thrombolysis

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Heparin-platelet factor 4 (PF4) antibodies mediate heparin-induced thrombocytopenia (HIT) and, irrespective of thrombocytopenia, are associated with poorer outcomes in some patients. The prevalence of heparin-PF4 antibodies, including platelet-activating ones, in patients in the medical, neurotrauma, or shock-trauma intensive care unit (ICU) remains unclear. In this single-center, observational study, heparin-PF4 antibodies (IgG/A/M) were measured by ELISA in 185 adults (median APACHE II score, 16) admitted to the medical (n = 27), neurotrauma (n = 96), or shock-trauma (n = 62) ICU and after 7 +/- 2 days. Seropositive patients and heparin-treated patients with unexplained, new-onset thrombocytopenia were also tested for platelet-activating antibodies using a serotonin release assay (SRA). Of 185 patients, seropositivity occurred in 20 patients (10.8%; 95% CI 6.7-16.2%) at admission and 54 (29.2%, 95% CI 22.8-36.3%) after 7 days (P < 0.001). Platelet-activating antibodies occurred in 4 seropositive patients at admission and 9 seropositive patients after 7 days (including in 1 patient at each assessment), each without thrombocytopenia or new thrombosis. Of 12 seropositive patients with platelet-activating antibodies, 6 had an ELISA optical density (OD) >1.0. ELISA-positive, SRA-negative, suspected HIT occurred in 1 patient. Heparin-PF4 antibodies are present in 10.8% of medical, neurotrauma, or shock-trauma ICU patients at admission and increase significantly to 29.2% within 7 days. Approximately 17-20% of seropositive ICU patients, often those with an ELISA OD >1.0, have platelet-activating heparin-PF4 antibodies.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Heparin–platelet factor 4 antibodies in intensive care patients: an observational seroprevalence study

Levine

Hergenroeder²,

Francis

et al. 2009

J Thromb Thrombolysis

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“…In regard to disease specific impacts on HIT, comprehensive and reliable data mainly exist based on patient series from cardiac surgery [17] , orthopedic surgery [18] , and vascular surgery [19,20] . However, reports and systematic studies on HIT in solid organ transplant recipients are rare and inconclusive.…”

Section: Introductionmentioning

confidence: 99%

Heparin-induced thrombocytopenia in solid organ transplant recipients: The current scientific knowledge

Aßfalg

Hüser

2016

WJT

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Exposure to heparin is associated with a high incidence of immunization against platelet factor 4 (PF4)/heparin complexes. A subgroup of immunized patients is at risk of developing heparin-induced thrombocytopenia (HIT), an immune mediated prothrombotic adverse drug effect. Transplant recipients are frequently exposed to heparin either due to the underlying end-stage disease, which leads to listing and transplantation or during the transplant procedure and the perioperative period. To review the current scientific knowledge on antiheparin/PF4 antibodies and HIT in transplant recipients a systematic PubMed literature search on articles in English language was performed. The definition of HIT is inconsistent amongst the publications. Overall, six studies and 15 case reports have been published on HIT before or after heart, liver, kidney, and lung transplantation, respectively. The frequency of seroconversion for anti-PF4/heparin antibodies ranged between 1.9% and 57.9%. However, different methods to detect anti-PF4/heparin antibodies were applied. In none of the studies HIT-associated thromboembolic events or fatalities were observed. More importantly, in patients with a history of HIT, reexposure to heparin during transplantation was not associated with thrombotic complications. Taken together, the overall incidence of HIT after solid organ transplantation seems to be very low. However, according to the current knowledge, cardiac transplant recipients may have the highest risk to develop HIT. Different alternative suggestions for heparin-free anticoagulation have been reported for recipients with suspected HIT albeit no official recommendations on management have been published for this special collective so far. Core tip: Heparin-induced thrombocytopenia (HIT) Ⅱ is a life-threatening complication of heparin therapy. Transplant recipients frequently are exposed to high doses of heparin before, during, and after transplantation. This review gives a systematic overview MINIREVIEWS

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“…1,28 The presence of heparin-PF4 antibodies, especially in high titers and irrespective of the presence of thrombocytopenia or thrombosis, is associated with increased all-cause mortality and morbidity in a number of patient populations. 3,29 Studies have reported significantly higher hospital mortality rates after cardiac surgery 30 and a higher incidence of thrombotic events in vascular reconstruction 31 and orthopedic surgery patients. 20…”

Section: Epidemiology and Risk Factors For Hitmentioning

confidence: 99%

The identification and management of heparin-induced thrombocytopenia in the vascular patient

LaMuraglia

Houbballah

Laposata

2012

Journal of Vascular Surgery

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Heparin-induced thrombocytopenia (HIT) is a serious, acquired, prothrombotic disorder caused by an antibody response to the heparin-platelet factor 4 complex, which can precipitate arterial as well as venous thromboembolic complications. HIT should be suspected in patients exposed to heparin who present with an unexplained thrombosis or a significant drop in platelet count, or both. Once HIT is suspected or identified, there are specific approaches to its diagnosis and management, with emphasis on removal of all heparin compounds and administration of alternative nonheparin anticoagulants. Generally, HIT is a self-limiting syndrome that resolves when the antibody titers disappear. Patients should be anticoagulated for up to 6 months, depending on the clinical scenario; however, the management of patients with remote or recent HIT requiring a vascular procedure requires special considerations.

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The role of heparin-associated antiplatelet antibodies in the outcome of arterial reconstruction

Cited by 34 publications

References 26 publications

Heparin–platelet factor 4 antibodies in intensive care patients: an observational seroprevalence study

Heparin–platelet factor 4 antibodies in intensive care patients: an observational seroprevalence study

Heparin-induced thrombocytopenia in solid organ transplant recipients: The current scientific knowledge

The identification and management of heparin-induced thrombocytopenia in the vascular patient

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