Heparin induced thrombocytopenia: prevalence in India (original) (raw)
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…, 1994
Background: As clinical diagnosis of heparin-associated thrombocytopenia (HAT) is often difficult, confirmation by sensitive laboratory assays is desirable. Stud Design and Methods: The sensitivity of the heparin-induced platelet activation (LIPA) test and the platelet aggregation test (PAT) was prospectively compared by using the sera of 209 patients with the putative diagnosis of HAT. Both assays were performed concomitantly with platelets of the same four donors using a different combination of donors from day to day. Further, all sera were assessed with a platelet factor 4 (PF4)/heparin enzyme-linked immunosorbent assay (ELISA). Results: Positive results were obtained with 33 percent of sera in the PFWheparin ELISA, with 33.5 percent of sera in the HlPA test, and with 11.5 percent of sera in the PAT. The PF4/heparin ELISA and the HlPA test showed no difference in sensitivity (p = 0.27 by McNemar's test) and were more sensitive than PAT (~4 0 " by McNemar's test). However, they recognized different patient cohorts. Nine HIPAindeterminate and 12 HIPA-negative sera were positive in the PFWheparin ELISA. Eight of the nine indeterminate sera caused platelet activation with high he arin concentrations in the HlPA test. Eleven of the 12 negative sera contained no LG, but 9 contained I M and 2 contained IgA HAT antibodies. Four sera that were indeterminate in the bF4,heparin ELISA and 18 sera that were negative were positive in the HlPA test. None of the sera that were positive in the PAT was missed in the HlPA test, but two of those were negative in the PFUheparin ELISA. All sera were assessed with four low-molecular-weight heparins and a low-molecular-weight heparinoid in the HlPA test with platelets from the same four donors. Low-molecular-weight heparin caused platelet activation with positive sera in 98 percent of tests, and the heparinoid did so in 10 percent; in a further 12.8 percent, crossreactivity to the low-molecular-weight heparinoid could not be excluded. Conclusion: The majority of HAT antibodies react with a PFWheparin complex, but there is stron evidence that other antigens are involved in some patients.The HlPA test and the jF4iheparin ELSA are sensitive for diagnosing HAT, and they complement one another. TRANSFUSION 1994;34:381-385. Abbreviations: ELSA = enzyme-linked lmmunosorbent assay; HAT = heparln-assoclated thrombocytopenia; HIPA = heparln-induced platelet activation (test); LMW = low molecular weight; PAT = platelet aggregation test; PF4 = platelet factor 4; SRA = serotonin-release assay.
Thrombocytopenia in the antiphospholipid syndrome
Annals of the Rheumatic Diseases, 1997
To determine the prevalence of thrombocytopenia in a group of patients suffering from the antiphospholipid syndrome (APS) and to investigate whether these patients may have any particular clinical or serological features. Retrospective analysis. A group of 171 APS patients seen in our department were studied for the presence of thrombocytopenia. Clinical and serological features of these patients were analysed by standard methods and each of them was correlated to the presence of thrombocytopenia and compared with those found in the group without thrombocytopenia. Each of the patients studied had a minimum of three platelet counts during the follow up period. Forty (23.4%) were found to have thrombocytopenia; 13 with persistently low and 27 patients with intermittently low platelet counts. There were no statistically significant differences in sex, age, disease duration or diagnosis when compared with the group of APS patients without thrombocytopenia. Thrombocytopenia was associated with thrombosis in 18, with miscarriages in five, and with both of these features in 13 patients. It was the only manifestation of the APS in four patients. All patients had persistently positive tests for antiphospholipid antibodies concomitantly with the low platelet counts. No significant association was found between the presence of thrombocytopenia and clinical or serological manifestations in APS patients. This study showed a prevalence of thrombocytopenia of 23.4% in APS. These patients did not present any significant clinical or serological features that distinguish them from those patients without thrombocytopenia.
Transfusion, 1994
Background: As clinical diagnosis of heparin-associated thrombocytopenia (HAT) is often difficult, confirmation by sensitive laboratory assays is desirable. Stud Design and Methods: The sensitivity of the heparin-induced platelet activation (LIPA) test and the platelet aggregation test (PAT) was prospectively compared by using the sera of 209 patients with the putative diagnosis of HAT. Both assays were performed concomitantly with platelets of the same four donors using a different combination of donors from day to day. Further, all sera were assessed with a platelet factor 4 (PF4)/heparin enzyme-linked immunosorbent assay (ELISA). Results: Positive results were obtained with 33 percent of sera in the PFWheparin ELISA, with 33.5 percent of sera in the HlPA test, and with 11.5 percent of sera in the PAT. The PF4/heparin ELISA and the HlPA test showed no difference in sensitivity (p = 0.27 by McNemar's test) and were more sensitive than PAT (~4 0 " by McNemar's test). However, they recognized different patient cohorts. Nine HIPAindeterminate and 12 HIPA-negative sera were positive in the PFWheparin ELISA. Eight of the nine indeterminate sera caused platelet activation with high he arin concentrations in the HlPA test. Eleven of the 12 negative sera contained no LG, but 9 contained I M and 2 contained IgA HAT antibodies. Four sera that were indeterminate in the bF4,heparin ELISA and 18 sera that were negative were positive in the HlPA test. None of the sera that were positive in the PAT was missed in the HlPA test, but two of those were negative in the PFUheparin ELISA. All sera were assessed with four low-molecular-weight heparins and a low-molecular-weight heparinoid in the HlPA test with platelets from the same four donors. Low-molecular-weight heparin caused platelet activation with positive sera in 98 percent of tests, and the heparinoid did so in 10 percent; in a further 12.8 percent, crossreactivity to the low-molecular-weight heparinoid could not be excluded. Conclusion: The majority of HAT antibodies react with a PFWheparin complex, but there is stron evidence that other antigens are involved in some patients.The HlPA test and the jF4iheparin ELSA are sensitive for diagnosing HAT, and they complement one another. TRANSFUSION 1994;34:381-385. Abbreviations: ELSA = enzyme-linked lmmunosorbent assay; HAT = heparln-assoclated thrombocytopenia; HIPA = heparln-induced platelet activation (test); LMW = low molecular weight; PAT = platelet aggregation test; PF4 = platelet factor 4; SRA = serotonin-release assay.
A systematic review of secondary thromboprophylaxis in patients with antiphospholipid antibodies
Arthritis & Rheumatism, 2007
To systematically review the efficacy and safety data of different therapeutic approaches in patients with antiphospholipid antibodies (aPL) and thrombosis. The Medline database and references from selected reports and review articles were used. Randomized controlled trials, prospective and retrospective cohort studies, and subgroup analysis (n > 15) that focused on the secondary thromboprophylaxis in patients with aPL were selected. Sixteen studies were selected. Patients with venous events and a single test for aPL showed a low recurrence rate while receiving oral anticoagulation at a target international normalized ratio (INR) of 2.0-3.0. Patients with stroke and a single positive aPL test had no increased risk compared with those without aPL. Recurrence rates in patients with definite antiphospholipid syndrome (APS) and previous venous thromboembolism were lower than in patients with arterial and/or recurrent events, both with and without therapy. Only 3.8% of recurrent events occurred at an actual INR >3.0. Mortality due to recurrent thrombosis was higher than mortality due to bleeding (18 patients versus 1 patient reported). For patients with definite APS, we recommend prolonged warfarin therapy at a target INR of 2.0-3.0 in APS patients with first venous events and >3.0 for those with recurrent and/or arterial events. For patients with venous thromboembolism or stroke and a single positive aPL test, we recommend further testing to determine if they have a persisting antibody. If they do not, the same therapy as for the general population should be used (warfarin at a target INR of 2.0-3.0 and low-dose aspirin, respectively).
Primary thromboprophylaxis with low-dose aspirin and antiphospholipid antibodies: Pro's and Con's
Autoimmunity Reviews, 2017
Whether primary prophylaxis should be prescribed in individuals with antiphospholipid antibodies (aPL) remains controversial due to the lack of relevant evidence-based data. Indeed, it is unclear whether the benefit of LDA outweighs the risk of major bleeding associated LDA in a low-risk population. On the contrary, stratification of aPL-positive subjects according to their aPL profile (combination, isotype and titer), presence of other concomitant risk factors for thrombosis and coexistence of an underling autoimmune disease is essential to decide whether primary prophylactic therapy should be prescribed. Additionally, the management of modifiable thrombotic risk factors is a necessary strategy, and the use of transient prophylaxis is crucial during high-risk periods. Specifically designed prospective trials are urgently needed to determine the real prophylactic impact of aspirin, as well as of alternative or concomitant therapeutic strategies such as hydroxychloroquine, statins or DOACS in aPL positive patients.
Clinical Significance of Positive Platelet Immunofluorescence Assay in Adult Immune Thrombocytopenia
Indian Journal of Hematology and Blood Transfusion, 2014
Immune thrombocytopenia (ITP) is a relatively common hematologic disorder manifested by low platelet count due to immune-mediated platelet destruction and/or suppression of platelet production. This study aim was to evaluate characteristics and clinical presentation of adult patients with ITP and exploring the clinical value of platelet antibodies assay in proposed cases in Iranian population. In this prospective case series 46 adult patients with ITP and platelet count of \100 9 10 9 /L, referred to the Taleghani Medical Center, Tehran, Iran between 2007 and 2009 were evaluated. There were 26 females and 20 males (1.3:1) with mean age of 38.9 ± 19.7 years. The platelet autoantibodies were measured by means of indirect platelet suspension immunofluorescence test. According to our results, 7 patients (15.2 %) displayed a positive platelet antibody assay. There was a significant negative correlation between platelet count and antibody level (r =-0 0.59; p \ 0.001). Additionally, a positive correlation between platelet count and patients' age (r = 0.302; p = 0.042) was detected. 20 patients (56.5 %) were symptomatic at presentation and the most common bleeding signs were petechia, purpura and epistaxis. Results indicated no significant correlation between increased platelet antibody level and bleeding manifestations except for hematuria (r = 0.435; p = 0.02) and epistaxis (r = 0.382; p = 0.015). Disclosure of platelet autoantibodies and the consequential thrombocytopenia associated to some extent but not completely with the propensity to bleed which necessitates more factors to be evaluated.
Journal of Laboratory and Clinical Medicine, 2006
Inhibition of erythrocyte (RBC) promotion of platelet reactivity could improve the antiplatelet effect of aspirin (ASA). We tested different ASA regimens for optimal inhibition of platelets and the effects of RBC in patients with a history of vascular diseases. Collagen-induced platelet activation (14 C-5HT, TXA 2 release) and platelet recruitment (proaggregatory activity of cell-free releasates from activated platelets) were measured in PRP, platelet-RBC (Hct 40%) and whole blood (WB) in 206 patients initially on 200-300 mg ASA/day. Their regimen was modified to biweekly 500 mg (loading dose, L) plus daily or twice-daily low-dose ASA (50 or 100 mg). TXA 2 was inhibited with all regimens. Percentage of patients with suboptimal inhibition of platelet recruitment in WB was: 200-300 ASA/ day (41%), L-50/day (87%), L-100/day (58%), L-50/twice-daily (39%) and L-100/twice-daily (20%; p<0.05 vs. other regimens). 14 C-5HT release was inhibited to the greatest extent with L-100/twicedaily in PRP+RBC or WB (p<0.05 vs. other regimens) due to greater inhibition of the RBC prothrombotic effect. Compared to other ASA regimens, L-100 twice-daily (equivalent to 221 mg ASA/day in the 14 day cycle), reduced by >50% the proportion of patients with suboptimal inhibition of platelet recruitment in WB and inhibited 14 C-5HT release to the greatest extent.
The Significance and Management of Thrombocytopenia in Antiphospholipid Syndrome
Current Rheumatology Reports, 2015
The association between antiphospholipid antibodies (aPL) and clinical problems goes beyond what is stated in the antiphospholipid syndrome (APS) classification criteria, namely thrombosis and pregnancy morbidity, and thrombocytopenia is the most common non-criteria hematologic manifestation of aPL with a frequency ranging from 20 to 50 %. Thrombocytopenia is rarely severe, and hemorrhage is far less common than thrombosis. However, when anticoagulation is considered, it may constitute a clinical problem with increased bleeding risk. Furthermore, thrombocytopenia represents a risk factor for thrombosis in aPL-positive patients. Therefore, it is important to understand the pathogenesis and the clinical associations of thrombocytopenia to build the right medical approach in aPL-positive patients. In this paper, we review the literature on aPL/APS-associated thrombocytopenia and briefly discuss the other conditions that can result in thrombocytopenia as they have commonalities with APS and their recognition is important to establish the most appropriate treatment strategy. Keywords Thrombocytopenia. Antiphospholipid syndrome. Immune thrombocytopenia. Antiphospholipid antibody. Thrombotic thrombocytopenic purpura. Heparin-induced thrombocytopenia. HELLP. Pre-eclampsia This article is part of the Topical Collection on Antiphospholipid Syndrome