High levels of heparin-platelet factor 4 antibodies in patients with pseudothrombocytopenia: risk of misdiagnosis

Martin-Toutain, Isabelle; Settegrana, Catherine; Ankri, Annick

doi:10.1111/j.1538-7836.2009.03493.x

Cited by 9 publications

(7 citation statements)

References 12 publications

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“…However, an important shortcoming of the assay is its limited specificity [86]. False-positive results are common and may result from detection of non-pathogenic anti-PF4/heparin antibodies [87,88] or anti-PF4 antibodies in patients with antiphospholipid syndrome and systemic lupus erythematosus [89]. A review of one institution's experience suggested that use of the polytypic ELISA alone was associated with the potential to overdiagnose HIT by as much as 100%, i.e.…”

Section: Immunologic Assaysmentioning

confidence: 96%

Heparin-induced thrombocytopenia: present and future

Cuker

2011

J Thromb Thrombolysis

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Heparin-induced thrombocytopenia (HIT) is a prothrombotic and potentially devastating complication of heparin therapy due to formation of platelet-activating antibodies against complexes of platelet factor 4 and heparin. Over the last several decades, great advances in our understanding of HIT have elevated a once enigmatic syndrome, the mere existence of which was doubted by the medical community, to a well-characterized disorder. Nevertheless, critical questions remain unanswered. The objective of this review is to examine our current understanding of the epidemiology, pathophysiology, diagnosis, and management of HIT and to highlight areas of future inquiry.

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Section: Immunologic Assaysmentioning

confidence: 96%

Heparin-induced thrombocytopenia: present and future

Cuker

2011

J Thromb Thrombolysis

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“…Additional conditions found to be especially associated with PTCP are reported in the scientific literature as case reports. These basically include viral infections [3,59,79], sepsis [80], thrombotic and cardiovascular disorder, heparin-induced thrombocytopenia (HIT) [41,81,82], auto-immune disorders [39,83], liver diseases [51,84], cancer [85,86], surgical settings [87][88][89], post stem cell transplantation [90,91], treatment with valproic acid [51], insulin, antibiotics [92], or chemotherapeutic agents such as sunitinib [52]. Some authors prefer to use the term "coincidental PTCP" or "concomitant PTCP" rather than expressly associating this condition with a particular disease [43,81].…”

Section: Clinical Risk Factorsmentioning

confidence: 99%

Pseudothrombocytopenia—A Review on Causes, Occurrence and Clinical Implications

Lardinois

Favresse

Châtelain

et al. 2021

JCM

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Pseudothrombocytopenia (PTCP), a relative common finding in clinical laboratories, can lead to diagnostic errors, overtreatment, and further (even invasive) unnecessary testing. Clinical consequences with potential life-threatening events (e.g., unnecessary platelet transfusion, inappropriate treatment including splenectomy or corticosteroids) are still observed when PTCP is not readily detected. The phenomenon is even more complex when occurring with different anticoagulants. In this review we present a case of multi-anticoagulant PTCP, where we studied different parameters including temperature, amikacin supplementation, measurement methods, and type of anticoagulant. Prevalence, clinical risk factors, pre-analytical and analytical factors, along with clinical implications, will be discussed. The detection of an anticoagulant-dependent PTCP does not necessarily imply the presence of specific disorders. Conversely, the incidence of PTCP seems higher in patients receiving low molecular weight heparin, during hospitalization, or in men aged 50 years or older. New analytical technologies, such as fluorescence or optical platelet counting, will be soon overturning traditional algorithms and represent valuable diagnostic aids. A practical laboratory approach, based on current knowledge of PTCP, is finally proposed for overcoming spuriously low platelet counts.

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“…In 2009, Martin-Toutain et al (6), prompted by the recognition of a heparintreated patient who developed pseudothrombocytopenia with a strong-positive PF4/heparin-EIA (but negative platelet aggregometry and no clinical features of HIT), systematically investigated sera from 15 patients with EDTA-induced pseudothrombocytopenia (but without a history of HIT or of heparin therapy) for anti-PF4/heparin antibodies in the Stago Dear Sirs, In general, two enzyme families are responsible for cyclic guanosine monophosphate (cGMP) synthesis; the soluble guanylyl cyclase (sGC) and particulate guanylyl cyclases (pGCs). sGC is a heterodimeric protein that consists of two homologous subunits (α and β) and it is the most sensitive receptor for nitric oxide (NO) (1).…”

Section: Lettersmentioning

confidence: 99%

“…NP receptors are expressed in the cardiovascular system (cardiac myocytes, endothelial and smooth muscle cells) and are involved in the regulation of numerous cardiovascular functions (4). Among blood cells, dendritic cells (5) and macrophages (6) have been shown to express GC-A and to respond to ANP with an increase of intracellular cGMP. In several publications, expression and function…”

Section: Lettersmentioning

confidence: 99%