Heparin-Associated Thrombocytopenia

King, Derek J.

doi:10.7326/0003-4819-100-4-535

Cited by 443 publications

(168 citation statements)

References 42 publications

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“…Stored serum collected from Cases 2 and 3 immediately before they began therapeutic doses of heparin revealed that these antibodies were already present, the result of exposure to heparin flushes during the previous 3 weeks. This presensitization was consistent with the immediate fall in platelet count following initiation of the higher dose of heparin in Case 2 [19].…”

Section: A S E R E P O R T : H E P a R I N F L U S H E S A N D H I Tsupporting

confidence: 75%

Heparin‐induced thrombocytopenia (HIT) due to heparin flushes: a report of three cases

Kadidal

Mayo

Horne

1999

Journal of Internal Medicine

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Abstract. Kadidal VV, Mayo DJ, Horne MK (National Institutes of Health, Bethesda, MD 20892, USA) Heparin-induced thrombocytopenia (HIT) due to heparin flushes: a report of three cases (Case Report). J Intern Med 1999; 246: 325±329.Three cases of heparin-induced thrombocytopenia (HIT) are reported that were provoked by daily heparin flushes of central venous access devices.Each case had confounding features that delayed recognition of the problem. A review of the literature revealed only 29 previously reported cases of HIT secondary to heparin flushes. However, the true incidence of this problem is unknown. A high index of suspicion and confirmatory laboratory tests are necessary to make the diagnosis.

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Section: A S E R E P O R T : H E P a R I N F L U S H E S A N D H I Tsupporting

confidence: 75%

Heparin‐induced thrombocytopenia (HIT) due to heparin flushes: a report of three cases

Kadidal

Mayo

Horne

1999

Journal of Internal Medicine

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“…Therefore, the circulatory and excretory system of animals exposed to the medicinal plant may be adversely affected. Certain medicinal herbal preparations or convectional drugs or chemicals adversely affect various blood components [15,8]. Decrease or increase in cell counts and depletion of plasma constituents or their elevation beyond reference range could equally demonstrate haematoxicity [5].…”

Section: Discussionmentioning

confidence: 99%

Effect of oral administration of aqueous whole extract of Cassytha filiformis on haematograms and plasma biochemical parameters in rats

et al. 2007

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Introduction:We evaluated the sub-chronic toxicity of the aqueous herbal extract prepared from Cassytha filiformis and administered daily for 28 days at dose levels (250, 500, and 1000 mg/kg bw) in male wistar albino rats. The LD 50 of the aqueous extract was determined.Methods: The effects on body weights, organ weights, and certain haematological and plasma biochemical parameters were measured as indices of organ toxicity.Results: The aqueous extract did not affect plasma glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT); however, a significant reduction in alkaline phosphatase (ALP) level occurred in all the treated groups. It also did not affect the electrolytes (Naϩ, ClϪ and Kϩ), total and direct bilirubin, creatinine, and glucose level. The aqueous extract elicited hypercholesterolaemic effects, but it did not affect the Hb, WBC, RBC, PVC, platelets, MCH, MCHC, MCV levels and differential counts (lympocytes, neutrophils, monocytes, eosinophils and basophils). It also reduced the body weight gain and absolute weight of the kidneys. The relative weights of the heart and lungs in some animal groups were equally reduced. The acute toxicological evaluation of the plant extract revealed an oral LD 50 value greater than 500 mg/kg bw.Conclusion: This study suggests that aqueous extract of C. filiformis administered at normal therapeutic doses is not likely to produce severe toxic effects on some organs or haematological and biochemical indices in rats.

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“…To 140 µL of pre-warmed donor PRP, 220 µL of patient's heatinactivated PPP was added to a cuvette containing a stir bar, which was placed in the aggregometer (ChronoLog, Havertown, PA). To this, 40 µL of 2.5 U mL 1 of UFH was added (final UFH concentration = 0.25 U mL 1 ) and the aggregation response was monitored for up to 5 min. The test was considered positive for HIT, if there was >20% platelet aggregation response due to HPF4 antibodies as per the assay criteria.…”

Section: Heparin-induced Platelet Aggregation (Hipa)mentioning

confidence: 99%

“…Heparin induced thrombocytopenia (HIT) is emerging as an important complication not only of unfractionated heparins (UFH), but also of low molecular weight heparins (LMWH) which are widely used as antithrombotic agent for both therapeutic as well as surgical indications [1] . Ethnic variation in prevalence of HIT is known to exist [2] .…”

Section: Introductionmentioning

confidence: 99%

Heparin-PF4 Antibodies in Heparin Induced Thrombocytopenia: Its Relationship with FcgRIIa Polymorphism

Kannan¹,

Ahmad²,

Ahmad³

et al. 2005

American J. of Immunology

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Abstract:We did the pilot study, in an attempt to determine the prevalence of HIT in Indians and determine its relationship, if any, to FcγRIIa polymorphism, the occurrence of heparin-induced thrombocytopenia (HIT) was investigated in 33 Indian patients undergoing cardiovascular surgery (CVS) who received unfractionated heparin (UFH). Platelet counts were performed prior to the initiation of UFH therapy and 5-16 days, post-therapy. The fall in patients' platelet count >35% of the baseline value or <100,000 µL 1 was considered to be suggestive of HIT syndrome. Heparin-induced platelet aggregation (HIPA), Enzyme Linked Immunosorbant assay (ELISA) and Serotonin Release Assay (SRA) tests were performed in all the patients to detect the antibodies formed against the heparin and platelet factor 4 complex (H-PF4). DNA analysis for FcγRIIa polymorphism was done by allele specific PCR. Thrombocytopenia was found to be present in 10 (30%) patients. Of these, 5 patients were found to be positive by HIPA, ELISA and SRA tests. These 5 patients were considered to have classic HIT syndrome. One of these patients had bleeding while the others were asymptomatic. One of the HIT positive patients was found to be homozygous for FcγRIIa His/ His polymorphism and others were heterozygous, had one defective allele with single amino acid change (Arg 131 His) at FcγRIIa platelet receptor. Frequency of occurrence of homozygous (FcγRIIa His/ His) and heterozygous (FcγRIIa Arg/ His ) polymorphism was higher in patients with HIT (100%) than in the normal population (68%). The prevalence of HIT in the pilot study (15%) was higher than that in the west (5%) but comparable to that from Japan (12%) (14). However, the Occurance of FcγRIIa polymorphism in Indian (68%) was higher than in the east (51%) and comparable to that in the west (78%). Thus it appears that the FcγRIIa polymorphism may have some relation to occurrence of HIT. Higher prevalence of FcγRIIa polymorphism in Indian may predispose to higher prevalence of HIT in India. Thus, it is recommended that, heparin-treated patients should be routinely tested for not only aPTT but also for platelet count, HPF4 antibodies and FcγRIIa polymorphism analysis. From the pilot study, it shows that absence of FcγRIIa receptor polymorphism may suggest low or negligible risk of development of HIT antibodies. However, further studies required with more patients using the same protocol.

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Heparin-Associated Thrombocytopenia

Cited by 443 publications

References 42 publications

Heparin‐induced thrombocytopenia (HIT) due to heparin flushes: a report of three cases

Heparin‐induced thrombocytopenia (HIT) due to heparin flushes: a report of three cases

Effect of oral administration of aqueous whole extract of Cassytha filiformis on haematograms and plasma biochemical parameters in rats

Heparin-PF4 Antibodies in Heparin Induced Thrombocytopenia: Its Relationship with FcgRIIa Polymorphism

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