P8: CHEMOTHERAPY INDUCED IMMUNE THROMBOCYTOPENIA-AN ENTITY TO KEEP IN MIND!

2016 ◽  
Vol 64 (3) ◽  
pp. 820.2-820
Author(s):  
P Draksharam ◽  
J Park ◽  
G Sidhu
Keyword(s):  
Flow Cytometry ◽  
Platelet Count ◽  
Recovery Time ◽  
Immune Thrombocytopenia ◽  
Chemotherapeutic Agents ◽  
Metastatic Colon Cancer ◽  
Platelet Recovery ◽  
Platelet Antibodies ◽  
Drug Dependent ◽  
Platelet Transfusions

Purpose of StudyThrombocytopenia during chemotherapy is not always due to myelosuppression. We report an unusual case of isolated acute thrombocytopenia after oxaliplatin and irinotecan administration. We reviewed 11 reported cases to better understand the nature of the presentation and variability in response to treatment.Case ReportPatient is a 63 year old female with metastatic colon cancer treated with palliative chemotherapy with FOLFOX. Follwing her 14th cycle she had an episode of acute drop in platelet count to 8,000/microliter. Peripheral smear revealed no evidence of thrombotic microangiopathy. She was managed with supportive platelet transfusions with slow recovery of platelet count. Subsequently she was treated with second line chemotherapy with FOLFIRI. Following the first cycle of Irinotecan, she again had a catastrophic drop in platelets from 136,000/microliter to 6,000/microliter within 10 hours. Due to this recurrent episode, a drug mediated thrombocytopenia was suspected and work up was initiated. She was initially treated with dexamethasone without a significant response. Platelet count normalized after 7 days with supportive platelet transfusions.Methods UsedBlood was tested for drug dependent platelet antibodies by Flow Cytometry at the Platelet and Neutrophil Immunology Laboratory at the Blood Center of Wisconsin.Summary of ResultsThe patient's serum showed evidence of drug dependent platelet antibodies to both oxaliplatin and irinotecan.ConclusionsDrug mediated immune thrombocytopenia is not uncommon. Time to severe acute thrombocytopenia and platelet recovery time varied post exposure of the drug. It is unclear whether steroid or IVIG administration had any effect on the platelet recovery time. Recovery from thrombocytopenia was observed in all 11 cases after the discontinuation of the insulting agent. Confirmation of the presence of drug dependent platelet antibodies against the chemotherapeutic agent by flow cytometry essential for diagnosis. This would be the first reported case of acute thrombocytopenia to two different chemotherapeutic agents in the same patient. Whether the reaction is two different mechanisms or if there is a cross reactivity between Oxaliplatin and Irinotecan has yet to be investigated.

Administration of Anti-Platelet Antibodies Prevents the Anti-Platelet Immune Response and Bleeding Complications of Neonatal Immune Thrombocytopenia in a Murine Model.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 223-223
Author(s):  
Heidi Tiller ◽  
Pingguo Chen ◽  
Bjorn Skogen ◽  
Mette Kjaer Killie ◽  
Anne Husebekk ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Immune Response ◽  
Platelet Count ◽  
Murine Model ◽  
Immune Thrombocytopenia ◽  
Human Platelet ◽  
Bleeding Complications ◽  
Platelet Antibodies ◽  
Β3 Integrin ◽  
Equity Ownership

Abstract Abstract 223 Background: The human platelet antigen (HPA) 1a is a potent immunogen located on the β3 integrin. Ten % of pregnant HPA1a negative women produce antibodies against the HPA1a antigen if the foetus is HPA1a positive. Fetal/neonatal immune thrombocytopenia (FNIT) can occur if the mother develops alloantibodies against fetal platelets, with intracranial haemorrhage as the most severe complication. The current opinion has been that immunization against the HPA1a antigen takes place during the first HPA1 non-compatible pregnancy. However, results from a large and recent screening study in Norway found that the majority (75%) of women were immunized around time of delivery, and not so often during pregnancy. This indicates that FNIT could be more similar to haemolytic disease of the newborn (HDN) than previously thought. To prevent HDN, antibody mediated immune suppression (AMIS) is induced by administration of anti-D antibodies in connection with RhD-negative pregnancies. The same principle could be used to prevent FNIT by administration of anti-HPA1a antibodies in HPA1a-negative pregnancies. We have previously established a murine model of FNIT using β3 integrin-deficient (β3−/−) mice. The first aim of the current project was to test whether administration of human anti-HPA1a IgG could suppress the anti-human platelet immune response in β3−/− mice after transfusion of human HPA1a positive platelets. For the second part of the project, we used a pure murine model to test whether administration of murine anti-β3 antibodies transfused after delivery could induce AMIS and prevent bleeding complications of FNIT in the subsequent pregnancies. Methods: Human/murine model: Human IgG from 5 donors with high levels of anti-HPA1a antibodies was purified by Protein G affinity chromatography. Purified IgG from one male donor without detectable anti-platelet specific antibodies was used as control IgG. Human platelets were isolated from an HPA1a positive donor. β3−/− mice were immunized by one tail vein transfusion with 2 × 106 human HPA1a positive platelets, with or without subsequent transfusion of 900ug human IgG (100% saturation). After 7 days, the mice were bled and sera collected. The anti-human platelet immune response was analyzed via flow cytometry, using FITC-conjugated goat anti-mouse IgG as detection antibody. Six mice were injected with anti-HPA1a containing IgG. Control IgG (n=6) or no IgG (n=4) were used as negative controls. Pure murine model: High-titer anti-β3 sera were produced by 4 weekly transfusions of 108 wild type (WT) platelets to β3−/− mice. Naïve β3−/− female mice were bred with naïve β3−/− male mice. Within 24 hours of delivery, the mother was transfused with 108 WT platelets with or without immediate transfusion of anti-β3 sera. The transfusions were repeated one week after delivery and the same females were bred again with WT male BALB/c mice. The anti-β3 immune response was analyzed via flow cytometry, using FITC-conjugated goat anti-mouse IgG. The FNIT phenotype was monitored and all live pups were bled from the carotid vein to determine platelet count. Results: Administration of purified anti-HPA1a IgG significantly suppressed the anti-human platelet immune response in β3−/− mice after transfusion of HPA1a positive platelets as compared with control IgG (p < 0.05). In the pure murine model of FNIT, the anti-β3 immune response was markedly suppressed during the subsequent pregnancy in the mice treated with anti-β3 sera. Two out of three mice receiving anti-β3 sera treatment delivered live pups with moderate thrombocytopenia without signs of haemorrhage (mean platelet count 217 ×106/mL). The third mouse receiving anti-β3 sera delivered dead pups. In contrast, all female mice (n = 3) without anti-β3 sera treatment miscarried. Conclusions: We have demonstrated in vivo that AMIS can be induced by administration of anti-platelet antibodies using a murine model of FNIT. Preliminary data indicates that bleeding complications of FNIT can be prevented with this prophylactic approach. Disclosures: Skogen: Prophylix Pharma a/s: Employment, Equity Ownership. Killie:Prophylix Pharma a/s: Equity Ownership. Husebekk:Prophylix Pharma a/s: Equity Ownership. Kjeldsen-Kragh:Prophylix Pharma a/s: Equity Ownership.

Dynamic Changes in Platelet Responsiveness to Thrombin and Coated Platelet Potential May Inform Risk of Hemorrhage and/or Thrombosis in a Novel Canine Mode of Immune Thrombocytopenia.

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 2193-2193
Author(s):  
Marshall A. Mazepa ◽  
Dana N LeVine ◽  
Adam J Birkenheuer ◽  
Marjory B Brooks ◽  
Shila K Nordone ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Platelet Count ◽  
Exploratory Study ◽  
Immune Thrombocytopenia ◽  
Treated Group ◽  
Canine Model ◽  
Severe Thrombocytopenia ◽  
Dynamic Changes ◽  
Platelet Recovery ◽  
Time Zero

Abstract Abstract 2193 In both canine and human patients with Immune Thrombocytopenia (ITP), bleeding risk is challenging to predict, and potentially leads to over-treatment of patients at low risk. Conversely, recent studies have highlighted the risk of thrombosis in ITP during platelet recovery. Given these clinical observations, we hypothesized that in ITP, changes in platelet response to agonists may occur in addition to changes in platelet numbers. In response to dual agonist activation (thrombin and convulxin), a subpopulation of platelets in both humans and dogs develops enhanced procoagulant activity. This subpopulation is termed coated platelets, and differences in individuals' potential to form coated platelets have been correlated with both hemorrhagic and thrombotic outcomes. In this exploratory study, we serially evaluated ex vivo platelet responsiveness to both thrombin and dual agonists (termed coated platelet potential) in a novel canine model of ITP. Dogs (n=4) were infused with a murine monoclonal anti-GPIIb antibody (2F9) in order to model ITP and generate predictable severe thrombocytopenia. Control dogs (n=3) were infused with a control antibody. Platelet count, thrombin responsiveness, and coated platelet potential were measured at baseline, time zero, 6 hours, 24 hours, and every 24hrs thereafter until the platelet count was ≥ baseline for at least two consecutive measures (recovery). Time zero was defined as the time when platelet count first fell to ≤ 30,000/μl following 2F9 infusion, or 1 hour following control antibody infusion. For platelet thrombin responsiveness, a monoclonal antibody to P-selectin was used to determine platelet P-selectin surface expression by flow cytometry after stimulation with graded doses of thrombin. The ED50 Thrombin was defined as the concentration of thrombin required for half-maximal P-selectin expression. Coated platelet potential was defined as the percent of platelets activated to the highly procoagulant state after dual stimulation with thrombin and convulxin, as determined by binding of biotinylated fibrinogen by platelets by flow cytometry. All dogs in the treated group developed severe thrombocytopenia (median=6×103, range=4–11×103 platelets/uL); no dogs in the control group developed thrombocytopenia. All treated dogs had platelet recovery by 240 hours (median=132 hours, range 120–240hours). Of interest, at 6 hours, ED50 Thrombin in the treated group increased nearly twofold (fig 1A) (ratio of median ED50 Thrombin treated/baseline=1.6, range 1.3–2.3), which correlated with a decline in coated platelet potential by nearly half of baseline (fig 1B) (median 52.4% of baseline, range 19.6–61.5%); minimal change from baseline was observed in controls. In both groups, ED50 Thrombin was lower at recovery than baseline (fig 1A) (treated median ED50 Thrombin=71.5% of baseline; control median ED50 Thrombin=67% of baseline). A trend of rising coated platelet potential was also noted as platelets recovered in the treated group. In conclusion, in this exploratory study of a canine model of ITP, we observed dynamic changes in platelet responsiveness. During severe thrombocytopenia, we observed a rise in ED50, indicating a decline in response to thrombin, which correlated with a fall in coated platelet potential. We speculate that this early fall in platelet thrombin response and coated platelet potential could contribute to hemorrhage risk in ITP. As a complement to this finding, in the treated group, there was a rise in coated platelet potential as platelets rebounded and coated platelet potential was slightly greater than baseline at recovery. This is consistent with others' observation that younger platelets are more likely to have coated platelet potential. We also observed a decline in ED50 Thrombin at recovery, not only in the treated dogs, but also control dogs. Thus, at recovery, the decline in ED50 Thrombin was independent of treatment group. However, this may be an artifact of our small sample size. Our observed increase in coated platelet potential during platelet recovery could potentially contribute to the thrombotic tendency of some ITP patients. Future studies are planned to explore the relationship of hemorrhagic and thrombotic risk with platelet thrombin responsiveness and coated platelet potential in this model of ITP and clinical studies of canine and human ITP. Disclosures: No relevant conflicts of interest to declare.

scholarly journals Detection of anti-platelet antibodies in immune thrombocytopenia by flow cytometry

2018 ◽  
Vol 184 (5) ◽  
pp. 844-847 ◽  
Author(s):  
Adrienn Teraz-Orosz ◽  
Nichola Cooper ◽  
James T.B. Crawley ◽  
Isabelle I. Salles-Crawley
Keyword(s):  
Flow Cytometry ◽  
Immune Thrombocytopenia ◽  
Platelet Antibodies

Thrombocytopenia after abciximab use results from different mechanisms

2010 ◽  
Vol 103 (03) ◽  
pp. 651-661 ◽  
Author(s):  
Gisèle Clofent-Sanchez ◽  
Pierre Coste ◽  
Paquita Nurden ◽  
Sophie Lajus ◽  
Catherine Jais ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Monoclonal Antibody ◽  
Flow Cytometry ◽  
Platelet Count ◽  
Time Dependent ◽  
Sensitive Test ◽  
Direct Elisa ◽  
Drug Dependent ◽  
Artery Disease ◽  
Antibody Specificities

SummaryOur study concerns thrombocytopenia in patients with acute ischaemic coronary artery disease receiving antiplatelet drugs to the αIIbβ3 inte-grin (GPIIb/IIIa). We have screened for drug-dependent antibodies (DDAB) in 18 patients who suffered a fall of > 50% in platelet count (9 patients had a nadir of <50,000 platelets/μl) after receiving abciximab and related results to clinical outcome. Serum or plasma was screened for DDAB using (i) a direct ELISA against purified αIIbβ3, αIIbβ3-abciximab complexes or abciximab alone, (ii) control platelets and flow cytometry and (iii) monoclonal antibody immobilisation of platelet antigens. DDAB were found for 11 patients, with αIIbβ3 ELISA the most sensitive test. Progressive platelet consumption linked with haemoglobin loss and/or use of intra-aortic balloon pumping, another potential cause of a fall in platelet count, was also evaluated. DDAB were identified that recognised αIIbβ3 associated with abciximab and/ or abciximab alone. Screening of both progressive and delayed thrombocytopenia (appearing after 5 to 11 days) suggested that antibodies against abciximab preceded those recognising neo-epitopes on αIIbβ3, with a time-dependent broadening of antibody specificities. Higher titres were seen after second abciximab use. Five antibodies were platelet-activating. In conclusion, the mechanisms responsible for this complication of anti-αIIbβ3 therapy are multiple and often associated with a complex immune response.

scholarly journals Antibodies in sulfonamide-induced immune thrombocytopenia recognize calcium-dependent epitopes on the glycoprotein IIb/IIIa complex

Blood ◽  
1994 ◽  
Vol 84 (1) ◽  
pp. 176-183 ◽  
Author(s):  
BR Curtis ◽  
JG McFarland ◽  
GG Wu ◽  
GP Visentin ◽  
RH Aster
Keyword(s):  
Flow Cytometry ◽  
Bovine Serum Albumin ◽  
Serum Albumin ◽  
Aqueous Medium ◽  
Bovine Serum ◽  
Immune Thrombocytopenia ◽  
Acetyl Derivative ◽  
Igg Antibodies ◽  
Calcium Dependent ◽  
Drug Dependent

Abstract Drug-dependent IgG antibodies (DDAb) induced by sulfamethoxazole (SMX) and sulfisoxazole (SIX) were identified by flow cytometry in 15 patients who developed thrombocytopenia while taking one of these medications. Fourteen of the 15 DDAb were specific solely for the glycoprotein (GP)IIb/IIIa complex, and 13 of these reacted wholly or in part with epitopes present only on the intact GPIIb/IIIa heterodimer. None of 12 SMX-induced DDAb cross-reacted with SIX, but one of three SIX-induced antibodies reacted with SMX. Each of 10 SMX-induced DDAb tested reacted with the N1-acetyl metabolite of SMX, but only one reacted fully with the N4-acetyl derivative. Detection of the SMX- and SIX-dependent antibodies was facilitated by using bovine serum albumin (BSA) to achieve suspension of these weakly soluble drugs in an aqueous medium. Our findings indicate that DDAb induced by SMX and SIX, in contrast to those induced by quinidine and quinine, are mainly specific for GPIIb/IIIa and react preferentially with calcium-dependent epitopes present only on the intact GPIIb/IIIa heterodimer.

The Significance of Anti-Platelet Antibodies Associated with Antibiotic Use, A Descriptive Analysis.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 4470-4470
Author(s):  
Ruta M Shah ◽  
Zbigniew M Szczepiorkowski ◽  
Miriam K Leach, MS, MT ◽  
Richard A Zuckerman
Keyword(s):  
Research Funding ◽  
Immune Thrombocytopenia ◽  
Solid Phase ◽  
Descriptive Analysis ◽  
Antibiotic Use ◽  
Bleeding Complications ◽  
Clear Understanding ◽  
Platelet Antibodies ◽  
Stop Date ◽  
Drug Dependent

Abstract Abstract 4470 Introduction Antibiotics (Abx) have been implicated in immune thrombocytopenia via drug dependent platelet antibodies (DDPA). Our institution has had a DDPA assay available since 1994 which is used to guide clinical decisions. We performed a retrospective review to determine the significance of DDPA. Methods We reviewed the medical records of patients (pts) who tested positive for abx DDPA between 1994 and 2006 and performed a descriptive analysis. Detection of DDPAs was performed using a previously described, modified solid phase red cell adherence assay that detects hapten or immune complex reactions. Results A total of 71 pts were included in this analysis. Multiple classes of abx were tested. Platelet nadir was &lt;50 in 70%, between 50 and 100 in 26% and over 100 in 4% of pts. Pts had between 1 and 4 abx tested: 37% had 1, 37% had 2, 15% had 3, and 11% had 4 tested; 65% of pts had one abx positive and 35% had &gt;1 abx positive for DDPA. Of those with &gt;1 abx tested (n=45), 14 (31%) had all tested abx positive. 53% of abx testing took place on or after the abx stop date and 32% of abx tested were administered for &lt;=3 days. Only 29 of 38 pts receiving heparin were tested for heparin-associated antibodies, and 14 had positive results. 49 pts had other non-abx drugs tested, 19 with positive DDPA. Thus, 35% had alternative non-abx testing positive for DDPA. 31% of pts had bleeding complications and 35% of pts died during hospitalization. Excluding pts who died and those with non-abx positive DDPA left 25 pts, median platelet counts were: abx start=142; nadir=22, abx discontinuation=46, hospital discharge=192. Conclusions Antibiotic DDPA testing is usually performed in ill pts with multiple medical complications and comorbidities. Abx were stopped for concern of DDPA in a number of pts for whom typical immune thrombocytopenia was not present or alternative explanations could be found. Though some pts exhibited improvement in platelet count after abx were stopped, a clear understanding of which pts may benefit from DDPA testing could not be determined based on the retrospective nature of this study and the complexity of pts histories. Further research is necessary to clarify the clinical applicability of DPPA testing. Disclosures: Szczepiorkowski: Cersus Corporation: Research Funding; CaridianBCT: Research Funding; BASF: Research Funding; Terumo Corporation: Research Funding; Fenwel, Inc - Scientific Advisory Board: Research Funding.

scholarly journals Helicobacter pylori eradication affects platelet count recovery in immune thrombocytopenia

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ayoung Lee ◽  
Junshik Hong ◽  
Hyunsoo Chung ◽  
Youngil Koh ◽  
Soo-Jeong Cho ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Platelet Count ◽  
Immune Thrombocytopenia ◽  
Complete Response ◽  
Long Term Effects ◽  
Infection Group ◽  
Platelet Recovery ◽  
First Line Therapy ◽  
H Pylori ◽  
Count Recovery

Abstract Helicobacter pylori (H. pylori) infection is on the rise as a cause of immune thrombocytopenia (ITP). It has been suggested that platelet recovery can be achieved following successful microbial eradication, although, the exact pathophysiology has yet to be fully elucidated. This study evaluated the long-term effects of H. pylori eradication monotherapy on platelet count recovery in patients with ITP. H. pylori eradication was analysed in 61 ITP patients. Patients who maintained a complete response (CR) for more than six months were classified as sustained responders (SR). The prevalence of H. pylori infection was 54.3% (75/138), and the success rate of eradication with first-line therapy was 71.4% (35/49). Patients who had achieved a CR at 2 months maintained a higher platelet count thereafter. At 1 year following eradication, platelet counts had increased 2.78 times in the eradicated group, 1.36 times in the sustained infection group, and 1.33 times in the no infection group compared with the baseline (P = 0.016).

scholarly journals Acute Immune-Mediated Thrombocytopenia due to Oxaliplatin and Irinotecan Therapy

2019 ◽  
Vol 2019 ◽  
pp. 1-5 ◽  
Author(s):  
Eric L. Tam ◽  
Padma L. Draksharam ◽  
Jennifer A. Park ◽  
Gurinder S. Sidhu
Keyword(s):  
Colon Cancer ◽  
Flow Cytometry ◽  
Severe Thrombocytopenia ◽  
Flow Cytometry Assay ◽  
Drug Induced ◽  
Advanced Colon Cancer ◽  
Platelet Antibodies ◽  
Immune Mediated ◽  
Drug Dependent ◽  
Underlying Mechanisms

We describe a case of a 63-year-old woman with advanced colon cancer and liver metastases who was treated with fluorouracil, leucovorin, and oxaliplatin (FOLFOX) and cetuximab chemotherapy. She tolerated 13 cycles of chemotherapy without any significant hematological side effects, but after the 14th cycle, she developed melena and was admitted for severe thrombocytopenia. After supportive care, the platelet counts rapidly improved to 76,000/μL. Upon initiation of FOLFIRI and cetuximab chemotherapy, she again developed rectal bleeding and severe thrombocytopenia with a platelet count of 6000/μL. Lab testing was positive for oxaliplatin and irinotecan drug-dependent platelet antibodies on flow cytometry assay. Drug-induced thrombocytopenia (DITP) is associated with several classes of drugs with several proposed underlying mechanisms. Prospective studies are needed to further address different mechanisms of drug-induced thrombocytopenia.

Severe vancomycin-induced thrombocytopenia in a patient with meningitis

2021 ◽  
Vol 14 (8) ◽  
pp. e244209
Author(s):  
Ian Savchenko ◽  
Tatiana Birg ◽  
Oleg Sharipov ◽  
Yulia Davydova
Keyword(s):  
Platelet Count ◽  
Antibiotic Treatment ◽  
Normal Values ◽  
Igg Antibodies ◽  
Vancomycin Therapy ◽  
Drug Induced ◽  
Drug Dependent ◽  
Hospital Acquired ◽  
Platelet Transfusions

Vancomycin is a widely used antibiotic and rarely can cause drug-induced thrombocytopenia. A patient with hospital-acquired meningitis after neurosurgery was treated with systemic and intrathecal vancomycin. On 9th day of antibiotic treatment, the patient’s platelets dropped to 0.68×109/L. Multiple platelet transfusions had minimal influence on platelet count. After cessation of vancomycin therapy, platelets returned to normal values without any additional interventions. Diagnosis of vancomycin-induced thrombocytopenia was confirmed by detection of drug-dependent antiplatelet IgG antibodies.

An Increase in the Immature Platelet Fraction Predicts Reconstitution of the Platelet Count and May Reduce Prophylactic Platelet Transfusions after Stem Cell Transplantation.

Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 3632-3632
Author(s):  
Samuel J. Machin ◽  
Dan Hart ◽  
Stefan Kunka ◽  
Carol Briggs ◽  
Laurence Corash
Keyword(s):  
Bone Marrow ◽  
Stem Cell ◽  
Platelet Count ◽  
Platelet Transfusion ◽  
Thrombocytopenic Purpura ◽  
Platelet Recovery ◽  
Transplant Patients ◽  
Automated Method ◽  
Immature Platelet Fraction ◽  
Platelet Transfusions

Abstract A new automated method to reliably quantitate reticulated platelets, expressed as the immature platelet fraction (IPF), has been developed on an automated cell counter (XE-2100, Sysmex). The IPF is identified by flow cytometery using a polymethine dye, staining platelet RNA, in the reticulocyte channel; the results are available at the same time as the CBC. The IPF normal range is 1.1–6.1%, mean 3.4%, 2 SD 2.3%. Reproducibility and stability results over 48 hours were acceptable. The IPF is raised when there is increased peripheral consumption/destruction. In untreated idopathic thrombocytopenic purpura, n = 12, mean 22.3%, range 9.2–33.1% and active thrombotic thrombocytopenic purpura, n = 5, mean 17.2%, range 11.2–30.9%. Patients who may require prophylactic platelet transfusion, usually at threshold counts less than 10 x 109/L, to support periods of marrow aplasia were monitored daily for platelet count and IPF%. The recovery phase of thrombocytopenia in most chemotherapy (n=13) and stem cell/bone marrow transplant patients (n=15) was preceded by a rise in IPF% several days prior to platelet recovery, mean IPF 13.7%, range 7–27.3%. In particular, patients undergoing autologous transplantation (n=8) using peripherally collected stem cells have a very characteristic IPF% motif, with a rise 1 day prior to engraftment for all patients except one where it was 2 days prior. For bone marrow derived transplant patients the increase in IPF was more variable, the rise preceded the rise in platelet count by 2–7days. These patients suffer more septic episodes where there is a rise in the IPF with no immediate increase in the platelet count, and require more regular platelet transfusions. Following a platelet transfusion there is a 24-hour transitory fall in the IPF response, which may impede platelet recovery. A parameter that could predict the timing of platelet recovery could be used clinically to reduce the use of prophylactic platelet transfusion in these patients, thus minimising donor exposure, infection risk and allowing substantial financial savings. The IPF is a useful parameter in the evaluation of the thrombocytopenic patient and has the potential to allow more optimal transfusion of platelet concentrates.

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