scholarly journals Platelet count recovery after intravenous immunoglobulin predicts a favorable outcome in children with immune thrombocytopenia

2016 ◽  
Vol 51 (2) ◽  
pp. 95 ◽  
Author(s):  
Hyoung Soo Choi ◽  
Mi Hong Ji ◽  
Sung Jin Kim ◽  
Hyo Seop Ahn
2020 ◽  
Vol 36 (6) ◽  
pp. 368-371
Author(s):  
Mohamed Fouad Selim ◽  
Manal Mohammad Ali Abdou ◽  
Ali Mohamed Ali Elnabtity

Author(s):  
snigdha nutalapati ◽  
gerhard hildebrandt

Vaccine mediated immune mediated thrombocytopenia (ITP) is an exceedingly rare. We present a 25-year-old female who developed severe refractory ITP with multiple active bleeding sites post second dose of COVID vaccination. She was treated with a combination of Romiplostim and Mycophenolate mofetil that resulted in rapid platelet count recovery.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ayoung Lee ◽  
Junshik Hong ◽  
Hyunsoo Chung ◽  
Youngil Koh ◽  
Soo-Jeong Cho ◽  
...  

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).


Blood ◽  
2002 ◽  
Vol 100 (6) ◽  
pp. 2087-2093 ◽  
Author(s):  
Ryan J. Hansen ◽  
Joseph P. Balthasar

Experiments were conducted to investigate the effects of intravenous immunoglobulin (IVIG) in a rat model of immune thrombocytopenia (ITP). Rats were pretreated with 0 to 2 g/kg IVIG and then challenged with an antiplatelet antibody (7E3, 8 mg/kg). IVIG effects on 7E3-induced thrombocytopenia and on 7E3 pharmacokinetics were determined. IVIG pretreatment led to significant changes in the degree and time-course of 7E3-induced thrombocytopenia (P = .031). Nadir percent platelet counts were 121% to 279% greater in animals treated with IVIG (0.4-2 g/kg) than in animals receiving 7E3 alone. IVIG treatment also led to dose-dependent increases in 7E3 clearance (P < .001), with more than 2-fold increases in 7E3 clearance seen following the highest dose of IVIG. In vitro experiments showed that IVIG effects on platelet count are not likely due to anti-idiotypic inhibition of 7E3-platelet binding and that IVIG did not directly bind to 7E3. Consequently, IVIG-7E3 binding cannot explain the increase of 7E3 clearance following IVIG treatment. We propose that the observed increase in 7E3 clearance with IVIG therapy is due to saturation of the FcRn salvage receptor for IgG. The importance of the effect of IVIG on 7E3 clearance to the prevention of thrombocytopenia in these animals is unclear at present; nonetheless, these data provide experimental support for a new mechanism of IVIG action in ITP (ie, IVIG-mediated increases in antiplatelet antibody elimination). This model of ITP will be useful for further investigations of IVIG mechanism of action and for development of new therapies for ITP.


2021 ◽  
Author(s):  
Ernesto Vigna ◽  
Daniele Caracciolo ◽  
Enrica Martino ◽  
Francesco Mendicino ◽  
Eugenio Lucia ◽  
...  

Abstract The discovery and the introduction of different vaccines in the therapeutic armamentarium against SARS-CoV-2 represents a big hope in the fight against the pandemic. However, safety of SARS-CoV-2 vaccination is continuously monitored for the emergence of potential new side effects, such as recently reported thrombotic events, after the use of certain types of vaccines. In this context, we report a case of 31-year-old woman who developed immune thrombocytopenia (ITP) after 3 weeks from receiving SARS-CoV-2 vaccine. She developed significant widespread petechiae and gum bleeding, with severe thrombocytopenia documented at her hemogram. Over a 10-day period, thrombocytopenia was treated first with high dose corticosteroids, intravenous immunoglobulin and platelet transfusions, without a platelet response. Two days later, she received the TPO-mimetic and after three days, his platelet count began to rise reaching the normal range 18 days from her admission to our Hematology department. These findings cannot actually elucidate if vaccination was causal or coincidental effect of ITP, but further highlights the need of additional pharmacovigilance studies to empower SARS-CoV2 vaccine efficacy.


Blood ◽  
2016 ◽  
Vol 128 (10) ◽  
pp. 1329-1335 ◽  
Author(s):  
Dongmei Sun ◽  
Nadine Shehata ◽  
Xiang Y. Ye ◽  
Sandra Gregorovich ◽  
Bryon De France ◽  
...  

Key Points Maternal platelet count response was not different for IVIg and corticosteroids in this retrospective study of pregnant women with ITP. Neonatal outcomes were overall favorable and similar after treatment of maternal ITP with IVIg or corticosteroids.


2020 ◽  
Vol 158 (6) ◽  
pp. S-244-S-245
Author(s):  
Ayoung Lee ◽  
Junshik Hong ◽  
Hyunsoo Chung ◽  
Youngil Koh ◽  
Soo-Jeong Cho ◽  
...  

Blood ◽  
2002 ◽  
Vol 100 (6) ◽  
pp. 2260-2262 ◽  
Author(s):  
Upendra P. Hegde ◽  
Wyndham H. Wilson ◽  
Therese White ◽  
Bruce D. Cheson

Fludarabine can exacerbate idiopathic thrombocytopenia (ITP) in chronic lymphocytic leukemia (CLL). We report 3 CLL patients with refractory fludarabine-associated ITP who responded to rituximab. The patients had Rai stages III, III, and IV disease. Before fludarabine treatment, the platelet counts were 141 000/μL, 118 000/μL, and 70 000/μL. ITP developed within week 1 of cycle 3 in 2 patients and within week 2 of cycle 1 in 1 patient. Platelet count nadirs were 4000/μL, 1000/μL, and 2000/μL, respectively, and did not respond to treatment with steroids or intravenous immunoglobulin. Rituximab therapy (375 mg/m2 per week for 4 weeks) was begun on days 18, 23, and 20 of ITP. Patient 1 achieved a platelet count of more than 50 000/μL at day 21 and more than 133 000/μL at day 28, patient 2 achieved a platelet count of more than 50 000/μL at day 4 and more than 150 000/μL at day 10, and patient 3 achieved a platelet count of more than 50 000/μL at day 5 and 72 000/μL at day 28 of rituximab therapy, with platelet response durations of 17+, 6+, and 6 months. These results suggest rituximab can rapidly reverse refractory fludarabine-associated ITP.


Blood ◽  
2002 ◽  
Vol 100 (6) ◽  
pp. 2260-2262 ◽  
Author(s):  
Upendra P. Hegde ◽  
Wyndham H. Wilson ◽  
Therese White ◽  
Bruce D. Cheson

Abstract Fludarabine can exacerbate idiopathic thrombocytopenia (ITP) in chronic lymphocytic leukemia (CLL). We report 3 CLL patients with refractory fludarabine-associated ITP who responded to rituximab. The patients had Rai stages III, III, and IV disease. Before fludarabine treatment, the platelet counts were 141 000/μL, 118 000/μL, and 70 000/μL. ITP developed within week 1 of cycle 3 in 2 patients and within week 2 of cycle 1 in 1 patient. Platelet count nadirs were 4000/μL, 1000/μL, and 2000/μL, respectively, and did not respond to treatment with steroids or intravenous immunoglobulin. Rituximab therapy (375 mg/m2 per week for 4 weeks) was begun on days 18, 23, and 20 of ITP. Patient 1 achieved a platelet count of more than 50 000/μL at day 21 and more than 133 000/μL at day 28, patient 2 achieved a platelet count of more than 50 000/μL at day 4 and more than 150 000/μL at day 10, and patient 3 achieved a platelet count of more than 50 000/μL at day 5 and 72 000/μL at day 28 of rituximab therapy, with platelet response durations of 17+, 6+, and 6 months. These results suggest rituximab can rapidly reverse refractory fludarabine-associated ITP.


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