A Cohort Study Investigating Compliance with Guidelines for Platelet Count Monitoring During Heparin Thromboprophylaxis

2012 ◽  
Vol 40 (2) ◽  
pp. 88-95
Author(s):  
Sunghye Kim ◽  
William E. Trick
Author(s):  
Mubashir H. Shah ◽  
Ramya Vedula ◽  
Reashma Roshan

Background: Thrombocytopenia as a side effect of phototherapy has not been mentioned in the standard literature but was described briefly as isolated case reports after the phototherapy came in vogue in 1958. The purpose of this study was to find the incidence of thrombocytopenia in neonates with uncomplicated indirect hyperbilirubinemia receiving phototherapy in a referral hospital.Methods: This was a prospective cohort study conducted in a referral hospital over a period of 18 months from June 1, 2013 to November 1, 2014.Results: A total of 103 babies were enrolled. The overall incidence of post-phototherapy thrombocytopenia was 45.6% while mild, moderate and severe thrombocytopenia was present in 66%, 21.3% and 12.8% of babies respectively. The lowest platelet count observed was 31,000/mm3 but none of the neonates showed bleeding manifestations. The incidence of thrombocytopenia following phototherapy was significantly higher in preterm babies, infants who received double surface phototherapy, babies who received phototherapy for >72 hours and in babies who received phototherapy on day 2 or 3 of life.Conclusions: Neonates requiring phototherapy for hyperbilirubinemia are at risk of developing thrombocytopenia, hence the treatment should be initiated based on the standard guidelines. Unnecessary use and prolongation of phototherapy should be avoided considering the possible side effects. Platelet count should be monitored particularly in pre-term neonates receiving phototherapy. Neonates receiving double surface phototherapy and those requiring phototherapy for longer duration require more frequent platelet count monitoring. 


2017 ◽  
Vol 24 (6) ◽  
pp. 944-949 ◽  
Author(s):  
Shinya Motohashi ◽  
Takefumi Matsuo ◽  
Hidenori Inoue ◽  
Makoto Kaneko ◽  
Shunya Shindo

Heparin-induced thrombocytopenia (HIT) is one of the serious complications in patients who undergo cardiac surgery. However, there remains a major problem in diagnosing HIT because the current immunological assays for detection of HIT antibody have limitations. Furthermore, the clinical course of thrombocytopenia in this surgery makes it increasingly difficult to diagnose HIT. We investigated the relationship between platelet count and HIT antibody in 59 patients who underwent cardiac surgery using cardiopulmonary bypass (CPB). The number of postoperative HIT antibody-positive patients evaluated using enzyme-linked immunosorbent assay kit (polyanion IgG/IgA/IgM complex antibodies/antiplatelet factor 4 enhanced) was 37 (62.7%). In contrast, platelet activation by HIT antibody was evaluated using the serotonin release assay (SRA). More than 20% and 50% release of serotonin was obtained from 12 patients (20.3%) and 8 patients (13.6%), respectively. The levels of d-dimer were significantly different on postoperative day 14 between SRA-positive and SRA-negative groups; however, postoperative thrombus complication was not detected using sonography in the patients with positive serotonin release at all. After being decreased by the operation, their platelet count recovered within 2 weeks in both groups equally. In our study, although the patients were positive in the platelet activating HIT antibody assay, they remained free from thrombosis and their platelet count recovered after early postoperative platelet decrease. Therefore, in addition to the SRA, monitoring of platelet count might be still considered an indispensable factor to facilitate the prediction of HIT thrombosis prior to manifestation in the patients undergoing cardiac surgery using CPB.


2018 ◽  
Vol 35 (6) ◽  
pp. 671-675 ◽  
Author(s):  
Emily Ankus ◽  
Sarah J Price ◽  
Obioha C Ukoumunne ◽  
William Hamilton ◽  
Sarah E R Bailey

Blood ◽  
2020 ◽  
Author(s):  
Paul A Kyrle ◽  
Sabine Eichinger

Cyclic thrombocytopenia (CTP) is a rare disease, which is characterized by periodic fluctuation of the platelet count. The pathogenesis of CTP is unknown and most likely heterogeneous. Patients with CTP are almost always misdiagnosed as having primary immune thrombocytopenia (ITP). The interval between ITP and CTP diagnosis can be many years. CTP patients often receive ITP-specific therapies including corticosteroids, thrombopoietin receptor agonists, rituximab and splenectomy which are followed by a transient increase in platelet count that is wrongly attributed to treatment effect with inevitable "relapse". CTP can be diagnosed by frequent platelet count monitoring which reveals a typical pattern of periodic platelet cycling. An early diagnosis of CTP will prevent these patients from being exposed to possibly harmful therapies. The bleeding phenotype is usually mild and consists of mucocutaneous bleeding at the time when the platelet count is at its nadir. Severe bleeding from other sites can occur but is rare. Some patients respond to cyclosporine A or to danazol, but most patients do not respond to any therapy. CTP can be associated with hematological malignancies or disorders of the thyroid gland. Nevertheless, spontaneous remissions can occur, even after many years.


2020 ◽  
pp. 115-115
Author(s):  
Nikola Pantic ◽  
Mirjana Mitrovic ◽  
Marijana Virijevic ◽  
Nikica Sabljic ◽  
Zlatko Pravdic ◽  
...  

During the current outbreak of Coronavirus disease 2019 (COVID-19), the way to manage patients with autoimmune diseases remains elusive due to limited data available. Case report: Addressing this issue we report a case of a COVID-19 positive 20-year-old female with prior history of Evans syndrome. She remained asymptomatic even though she had been treated with immunosuppressants (prednisolone and azathioprine) together with romiplostim. Moreover, her course of infection was accompanied by thrombocytosis, although her platelet count was mostly below the reference range before the infection. The patient was monitored vigilantly, with special regard to platelet count and signs of thrombotic events. Conclusion: Platelet count monitoring and romiplostim administration should be performed more cautiously in ITP patients infected by SARS-CoV-2.


2006 ◽  
Vol 24 (18_suppl) ◽  
pp. 8602-8602 ◽  
Author(s):  
J. Bussel ◽  
M. Saleh ◽  
D. Provan ◽  
N. Stone ◽  
J. M. Hamilton ◽  
...  

8602 Background: Eltrombopag (SB-497115) is a novel, first in class, orally bioavailable, thrombopoietin receptor agonist that induces differentiation and proliferation of megakaryocyte progenitors and has been shown to increase platelet counts in preclinical and clinical studies. Methods: In two randomized, placebo-controlled trials, eltrombopag was administered as oral tablets, once daily for 10 days to 73 healthy male subjects at doses of 5–75mg in an ascending dose cohort study, and to 103 (64 female/39 male) adult chronic immune thrombocytopenic purpura (ITP) patients, with a platelet count of <30×109/L, once daily for 6 weeks at doses of 30–75mg in a parallel dose cohort study. The primary efficacy endpoint in the Phase II ITP trial was the proportion of subjects with a platelet count >50×109/L after 6 weeks of dosing. Results: In healthy subjects, eltrombopag induced a dose dependent increase in the platelet counts. Mean maximal platelet count increases were 24.1 % at 30mg, 42.9 % at 50mg, and 50.4 % at 75mg. In 95 eligible ITP patients, platelet counts increased from <30 to >50×109/L in 16% (4/25) of subjects on placebo, and in the eltrombopag groups in 28% (7/25, p=ns) on 30mg, 67% (16/24, p<0.001) on 50mg and 86% (18/21, p<0.001) on 75mg eltrombopag. The median platelet counts in each treatment arm after 6 weeks of dosing were 16×109/L on placebo, 29×109/L on 30mg, 132×109L on 50mg, and 202×109/L on 75mg. The dose dependent effect was not significantly affected by the splenectomy status, background immunosuppressant use, or baseline platelet count (greater than or less than 15×109/L). Conclusions: The platelet count data from these clinical studies suggests that eltrombopag could be an effective therapy for the treatment of thrombocytopenia. Eltrombopag is being tested in further studies involving patients with ITP and chronic liver disease, and cancer patients receiving thrombocytopenic chemotherapy. [Table: see text]


Blood ◽  
2004 ◽  
Vol 104 (11) ◽  
pp. 4040-4040
Author(s):  
Jyoti Kotwal ◽  
G. S. Chopra ◽  
A. Kotwal ◽  
Y. V. Sharma ◽  
J. R. Bhardwaj

Abstract Thrombosis has been recognized as a complication of rapid ascent as well as long-term stay at high altitude (HA). Researchers have presented conflicting results and majority of them studied only short-term stay. A prospective cohort study was carried out at a height of 3500 m to study the hematological factors, which may lead to increased propensity to thrombosis on prolonged stay at HA. The subjects were healthy low landers (initial N=38, complete follow up N=32) in age group of 20–40 years, inducted to HA and investigated at induction and subsequently at 3 and 8 months. The comparison cohort was age and sex matched low landers not inducted to HA. Bleeding time, clotting time, hemoglobin (Hb), HCT, platelet count, prothrombin time, APTT, fibrinogen, d-dimers. Protein C, protein S, anti-thrombin III levels, APC resistance, PAI-1, Beta thromboglobulin (BTG) and PF4 were estimated. On induction to HA the mean Hb, platelet count, fibrinogen levels, PAI-1 levels and levels of platelet activation factors were in normal range and not statistically different from those at low altitude (P>0.05). None of the subjects had thrombophilia. There was no statistically significant change in Protein C, Protein S, AT III levels, APC resistance, BT, CT, PT and APTT. The mean values were: Hb (13.9, 15.6, 16.6 gm/dl); platelet count (255, 309, 343 x 103/mm3); fibrinogen (253, 304, 346 mg/dl); BTG (30.3, 38.5, 47.3 IU/ml); PF 4 (3.9, 7.6, 13.7 IU/ml) and; PAI-1 (23.7, 40.1, 49.3 ng/ml), at (induction, 3 months, 8 months) respectively. The P value for all was 0.000 by repeated measure analysis. The high Hb itself is unlikely to be the single cause of the thrombotic tendency at HA as its maximum value was 18.0 gm/dl. Erythrocytosis and hyper viscosity are known to activate platelets, however, platelet activation may be the result of hypoxic stress and injury to platelets or endothelium. An important finding of the study was the rise in PAI-1 levels that correlated with rise in fibrinogen levels and duration of stay at HA (Figure 1 and 2). The endothelial injury and clotting activation followed by increased fibrinolysis maintains homeostasis. We hypothesize that increased PAI-1 level tilts the balance by decreasing fibrinolytic activity and increasing propensity to thrombosis. Hypoxia during surgery is known to cause raised postoperative PAI-1 levels leading to a tendency of postoperative thrombosis. The prolonged hypoxia in a lowlander staying in HA may have a similar effect. By virtue of increased platelet count, hematocrit, platelet activation factors, PAI-1 and fibrinogen, prolonged stay at HA is a pro thrombotic state. Thus, there may be a role for antiplatelet drugs in prevention in view of the platelet hyperactivity and interventional trials with homocysteine lowering vitamins or aspirin also need to be considered.


2018 ◽  
Vol 2 (19) ◽  
pp. 2433-2442 ◽  
Author(s):  
Ada Gillissen ◽  
Thomas van den Akker ◽  
Camila Caram-Deelder ◽  
Dacia D. C. A. Henriquez ◽  
Kitty W. M. Bloemenkamp ◽  
...  

Abstract We describe the pattern of change in coagulation parameters during the course of severe postpartum hemorrhage in a retrospective cohort study among 1312 women experiencing severe postpartum hemorrhage necessitating blood transfusion. Levels of hemoglobin, hematocrit, platelet count, fibrinogen, activated partial thromboplastin time (aPTT) and prothrombin time (PT) per categorized volume of blood loss during severe postpartum hemorrhage were described and compared between women with and without the composite adverse outcome. Need for surgical intervention, severe acute maternal morbidity, and maternal mortality were jointly considered the composite adverse outcome. Of the 1312 women, 463 (35%) developed the composite adverse outcome. The incidence of a fibrinogen level &lt;2 g/L was 26% (342 per 1312). Low fibrinogen and prolonged aPTT during the first 2 L of hemorrhage were associated with a subsequent composite adverse outcome; median fibrinogen and aPTT among women with and without the composite end point after 1.5 to 2 L of hemorrhage were 1.5 g/L (interquartile range [IQR], 1.0-1.9) vs 2.7 g/L (IQR, 1.9-3.4) and 39 s (IQR, 30-47) vs 32 s (IQR, 28-36), respectively. PT and platelet count as assessed during the first 2 L of hemorrhage were not associated with morbidity or mortality. Our results suggest that detection of low levels of fibrinogen and elevated aPTT levels during early postpartum hemorrhage can contribute to the identification of women that may benefit from targeted hemostatic treatment. Essential in this identification process is the moment of reaching a level of fibrinogen of &lt;2 g/L during the course of postpartum hemorrhage.


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