Severe Immune Thrombocytopenia in Pregnancy: Intravenous Immunoglobulin Can Improve Platelet Count Significantly

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.

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

Blood Research ◽

10.5045/br.2016.51.2.95 ◽

2016 ◽

Vol 51 (2) ◽

pp. 95 ◽

Cited By ~ 4

Author(s):

Hyoung Soo Choi ◽

Mi Hong Ji ◽

Sung Jin Kim ◽

Hyo Seop Ahn

Keyword(s):

Platelet Count ◽

Intravenous Immunoglobulin ◽

Immune Thrombocytopenia ◽

Favorable Outcome ◽

Count Recovery

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Co-incidental Von Willebrands disease and immune thrombocytopenia in pregnancy: treatment with high dose intravenous immunoglobulin

Clinical & Laboratory Haematology ◽

10.1111/j.1365-2257.1986.tb00099.x ◽

1986 ◽

Vol 8 (3) ◽

pp. 227-231 ◽

Cited By ~ 1

Author(s):

D. Maharaj ◽

I.D. Walker ◽

H.P. Mcewan ◽

C.E. Nisbet ◽

J.G. Erskine

Keyword(s):

Intravenous Immunoglobulin ◽

Immune Thrombocytopenia ◽

High Dose ◽

In Pregnancy

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Acute thrombocytopenia: picking a way through a paucity of platelets

British Journal of Hospital Medicine ◽

10.12968/hmed.2019.80.9.507 ◽

2019 ◽

Vol 80 (9) ◽

pp. 507-512

Author(s):

E Nuttall Musson ◽

O Lomas ◽

MF Murphy

Keyword(s):

Platelet Count ◽

Adult Patient ◽

General Hospital ◽

Disseminated Intravascular Coagulation ◽

Immune Thrombocytopenia ◽

Underlying Disease ◽

Hospital Physician ◽

Case Histories ◽

Thrombocytopenic Purpura ◽

In Pregnancy

Thrombocytopenia is defined as a platelet count under 150x109/litre. It may be found as a bystander to other pathology or directly related to an underlying haematological condition. Apart from laboratory artefact, it should be treated seriously as it often reflects serious underlying disease. This review uses short case histories to illustrate how to approach thrombocytopenia during the initial presentation of an adult patient to hospital. This article guides the general hospital physician through the narrow but potentially confusing differential diagnoses related to thrombocytopenia, with particular focus on immune thrombocytopenia, disseminated intravascular coagulation and thrombotic thrombocytopenic purpura. Thrombocytopenia in pregnancy deserves special consideration and will not be discussed in this article.

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Thrombocytopenia in Pregnancy: Approach to Diagnosis and Management

Seminars in Thrombosis and Hemostasis ◽

10.1055/s-0040-1708842 ◽

2020 ◽

Vol 46 (03) ◽

pp. 256-263

Author(s):

Annemarie E. Fogerty

Keyword(s):

Platelet Count ◽

Immune Thrombocytopenia ◽

Thrombocytopenic Purpura ◽

Gestational Thrombocytopenia ◽

Life Threatening ◽

Immune Thrombocytopenia Purpura ◽

The Impact ◽

Underlying Pathophysiology ◽

In Pregnancy ◽

Management Issues

AbstractThe impact of thrombocytopenia varies widely depending on the underlying pathophysiology driving it. The biggest challenge in managing thrombocytopenia in pregnancy is accurately identifying the responsible pathophysiology—a task made difficult given the tremendous overlap in clinical and laboratory abnormalities associated with different thrombocytopenia processes. The most common etiologies of thrombocytopenia in pregnancy range from physiology deemed benign to those that are life-threatening to the mother and fetus. Even in cases in which the responsible etiology is deemed benign, such as gestational thrombocytopenia, there are still implications for the management of labor and delivery, a time where hemostatic challenges may prove life-threatening. In most institutions, a minimum platelet count will be mandated for epidural anesthesia to be deemed a safe option. The causes of thrombocytopenia can also include diagnoses that are pregnancy-specific (such as preeclampsia or gestational thrombocytopenia), potentially triggered by pregnancy (such as thrombotic thrombocytopenic purpura), or unrelated to or predating the pregnancy (such as liver disease, infections, or immune thrombocytopenia purpura). It is imperative that the source of thrombocytopenia is identified accurately and expeditiously, as intervention can range from observation alone to urgent fetal delivery. In this review, the approach to diagnosis and the pathophysiological mechanisms of the most common etiologies of thrombocytopenia in pregnancy and associated management issues are presented.

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Effects of intravenous immunoglobulin on platelet count and antiplatelet antibody disposition in a rat model of immune thrombocytopenia

Blood ◽

10.1182/blood.v100.6.2087.h81802002087_2087_2093 ◽

2002 ◽

Vol 100 (6) ◽

pp. 2087-2093 ◽

Cited By ~ 5

Author(s):

Ryan J. Hansen ◽

Joseph P. Balthasar

Keyword(s):

Platelet Count ◽

Intravenous Immunoglobulin ◽

Rat Model ◽

Immune Thrombocytopenia ◽

Time Course ◽

Ivig Therapy ◽

Ivig Treatment ◽

Antiplatelet Antibody ◽

Dose Dependent

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.

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A Case of Immune Thrombocytopenia After COVID-19 Vaccination: Coincidental or Causal Effect? Running Title: ITP After COVID-19 Vaccination

10.21203/rs.3.rs-448522/v1 ◽

2021 ◽

Author(s):

Ernesto Vigna ◽

Daniele Caracciolo ◽

Enrica Martino ◽

Francesco Mendicino ◽

Eugenio Lucia ◽

...

Keyword(s):

Platelet Count ◽

Side Effects ◽

Intravenous Immunoglobulin ◽

Vaccine Efficacy ◽

Immune Thrombocytopenia ◽

Causal Effect ◽

High Dose ◽

Severe Thrombocytopenia ◽

Platelet Response ◽

Normal Range

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.

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Immune thrombocytopenia in pregnancy

Fetal and Maternal Medicine Review ◽

10.1017/s0965539500000334 ◽

1990 ◽

Vol 2 (2) ◽

pp. 143-157 ◽

Cited By ~ 4

Author(s):

James Browning ◽

David James

Keyword(s):

Platelet Count ◽

Intracerebral Haemorrhage ◽

Intracranial Haemorrhage ◽

Immune Thrombocytopenia ◽

Autoimmune Thrombocytopenia ◽

Reliable Test ◽

Alloimmune Thrombocytopenia ◽

Route Of Delivery ◽

Abdominal Delivery ◽

In Pregnancy

Autoimmune thrombocytopenia (ITP)1) The risks to mother and fetus have previously been overstated.2) There is no maternal test which will accurately determine fetal thrombocytopenia.3) The only reliable test for fetal thrombocytopenia is cordocentesis – this carries a higher morbidity than that of fetal intracerebral haemorrhage from ITP.4) Contrary to received wisdom, there is no evidence that, even for the most severely thrombocytopenic infant, abdominal delivery protects against intracranial haemorrhage.5) Management therefore involves keeping the maternal platelet count above 50 × 1091 and choosing the route of delivery on normal obstetric grounds.Alloimmune thrombocytopenia1) Alloimmune thrombocytopenia is commoner than hitherto believed (0.15% all neonates).2) The fetal risks are considerable: intracranial haemorrhage occurs in 4% of cases antenatally and in 10% in labour. The risks are virtually confined to those with a platelet count of less than 30 × 109l−1.3) Cordocentesis is justified for the ‘at risk’ fetus; fetal immunoglobulin or platelet therapy can be given.4) When the fetal platelet count is below 50 × 109l−1, abdominal delivery should be planned.5) A maternal screening test for neonatal alloimmune thrombocytopenia exists (lack of P1A1 antigen).

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Rituximab treatment of refractory fludarabine-associated immune thrombocytopenia in chronic lymphocytic leukemia

Blood ◽

10.1182/blood.v100.6.2260.h81802002260_2260_2262 ◽

2002 ◽

Vol 100 (6) ◽

pp. 2260-2262 ◽

Cited By ~ 6

Author(s):

Upendra P. Hegde ◽

Wyndham H. Wilson ◽

Therese White ◽

Bruce D. Cheson

Keyword(s):

Platelet Count ◽

Chronic Lymphocytic Leukemia ◽

Intravenous Immunoglobulin ◽

Immune Thrombocytopenia ◽

Lymphocytic Leukemia ◽

Platelet Response ◽

Idiopathic Thrombocytopenia ◽

Platelet Counts

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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Rituximab treatment of refractory fludarabine-associated immune thrombocytopenia in chronic lymphocytic leukemia

Blood ◽

10.1182/blood.v100.6.2260 ◽

2002 ◽

Vol 100 (6) ◽

pp. 2260-2262 ◽

Cited By ~ 57

Author(s):

Upendra P. Hegde ◽

Wyndham H. Wilson ◽

Therese White ◽

Bruce D. Cheson

Keyword(s):

Platelet Count ◽

Chronic Lymphocytic Leukemia ◽

Intravenous Immunoglobulin ◽

Immune Thrombocytopenia ◽

Lymphocytic Leukemia ◽

Platelet Response ◽

Idiopathic Thrombocytopenia ◽

Platelet Counts

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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