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Physiologic Changes
Published in Vincenzo Berghella, Obstetric Evidence Based Guidelines, 2022
The performance of complete blood counts as a part of routine prenatal screening results in a frequent diagnosis of thrombocytopenia in asymptomatic pregnant women. The mean platelet count in pregnant women is lower than in nonpregnant women (average 213,000/µL), with 7%–12%% of pregnant women meeting criteria for the diagnosis of thrombocytopenia by delivery [27]. Manifestations of thrombocytopenia include epistaxis, petechiae, and ecchymosis, although frequently there are no clinically significant effects. Clinically significant spontaneous bleeding is rare except with exceptionally low platelet counts, and platelet transfusion is only recommended for surgery if platelet count is less than 50,000/µL [27]. The most common cause of thrombocytopenia in pregnancy is gestational thrombocytopenia, which is an apparently benign condition whose underlying physiology is not well understood. However, thrombocytopenia in pregnancy may also be caused by more severe underlying conditions such as preeclampsia, human immunodeficiency virus infection, immune thrombocytopenic purpura (ITP), systemic lupus erythematosus, antiphospholipid antibody syndrome, hypersplenism, disseminated intravascular coagulation, thrombotic thrombocytopenic purpura, hemolytic uremic syndrome, congenital thrombocytopenia, or medication effect [27]. Most of these conditions can be ruled out by history, physical exam, and exclusion of underlying diagnoses.
Pregnancy in SLE
Published in E. Nigel Harris, Thomas Exner, Graham R. V. Hughes, Ronald A. Asherson, Phospholipid-Binding Antibodies, 2020
Treatment of thrombocytopenia depends on diagnosis of its cause. If thrombocytopenia occurs in a pregnant woman who has not previously had thrombocytopenia as a manifestation of her SLE, who has no other signs of active SLE, who has high titer anti-cardiolipin antibody, or who has signs of placental insufficiency, and if the platelet count is >50,000/mm3, aspirin, 80 mg/d, usually reverses the thrombocytopenia. If other signs of active SLE are present, if the patient’s prior flares have been characterized by thrombocytopenia, or if the platelet count is <50,000/mm3, we use prednisone, 30 to 60 mg/d. In severe thrombocytopenia, intravenous gammaglobulin will transiently raise the platelet count to allow surgery, such as cesarean section. (There are reports that intravenous gammaglobulin may also be useful in treatment of aPL-associated fetal death.) Splenectomy is a drastic but sometimes necessary last resort.32,35,38Table 2 outlines suggested therapies for thrombocytopenia.
Immunoglobulins
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
The disease immune thrombocytopenic purpura (ITP) results from production of antiplatelet antibodies. IgG-coated platelets are phagocytosed by splenic macrophages leading to thrombocytopenia and a bleeding diathesis. The disorder is often self-limited and therapy is directed toward preventing prolonged profound thrombocytopenia. Standard therapy consists of intravenous immune globulin (see below). At least part of the therapeutic effect of gamma globulin infusion is due to saturating macrophage IgG FcR; this prevents phagocytosis of autoantibody-coated platelets. Antibodies directed specifically against FcγRIII have also been used to increase platelet life span in ITP.
Primary Immunodeficiency and Thrombocytopenia
Published in International Reviews of Immunology, 2022
Maryam Mohtashami, Azadehsadat Razavi, Hassan Abolhassani, Asghar Aghamohammadi, Reza Yazdani
Thrombocytopenia is characterized by a low count of platelet about less than 150 × 109/L in the blood. The causes of thrombocytopenia are divided into two categories non-immunologic and immunologic. In both categories, thrombocytopenia resulted from decreased platelet production and increased platelet destruction. Immune-mediated thrombocytopenia (ITP), is one of the most prevalent autoimmune and hematologic disorders among IEI patients [6]. ITP can be linked with several causes such as drug-induced thrombocytopenia (DITP), auto-immune diseases, infections-mediated/disseminated intravascular coagulation in sepsis, post-transfusion of blood products and due to autoreactive lymphocytes [7, 8]. ITP is induced by the immune response to GPIbα, GPIIb/IIIa and GPIa/IIa complex, antibody production and its clearance via the spleen [9]. Moreover, the destruction of megakaryocytic precursors by the immune system is another reason for ITP [10]. Contrary to ITP, studies have also revealed that Thrombotic Thrombocytopenic Purpura (TTP) resulted from increased platelet activation and aggregation which should be differentiated at the time of diagnosis [11].
Prevention and control strategies in the diagnosis and treatment of solid tumors in children during the COVID-19 pandemic
Published in Pediatric Hematology and Oncology, 2020
Jiabin Cai, Lili Zheng, Danni Lv, Min He, Jieni Xiong, Junqing Mao, Jinhu Wang
Chemotherapy is one of the most essential links in the comprehensive treatment of malignant solid tumors in children. During the pandemic, ensuring the standardization and continuity of the implementation of the chemotherapy plan is a key point to guarantee a curative effect. As mentioned above, most children will have myelosuppression of varying degrees and duration after chemotherapy. Leukopenia increases the risk of infection in children (including that of SARS-Cov-2); patients are prone to severe or even fatal infections in the case of neutropenia or lack of neutrophils. Severe thrombocytopenia may lead to fatal bleeding complications. During a pandemic, insufficiencies may occur in the supply of platelets and red blood cells, so it is necessary to emphasize standardization in the implementation of chemotherapy regimens during the pandemic to avoid the application of large-dose chemotherapy regimens and minimize the application of chemotherapy regimens to reduce the risk of severe myelosuppression. Long-acting granulocyte stimulating factor prevention is recommended for children who have been noted to be prone to severe granulocytopenia or deficiency during the previous course of treatment. Recombinant human thrombopoietin is recommended for children who have been prone to severe thrombocytopenia. If necessary, appropriately reducing the dose of chemotherapy should be considered to guarantee the safety of children in such unusual periods.
Myelodysplastic syndromes: a review of therapeutic progress over the past 10 years
Published in Expert Review of Anticancer Therapy, 2020
Jonathan Feld, Abigail Belasen, Shyamala C Navada
Severe thrombocytopenia can lead to life-threatening bleeding. Previously, thrombocytopenia was managed with platelet transfusions and HMAs. More recently, the thrombopoietin (TPO) mimetics, romiplostim and eltrombopag, have been studied for use in patients with MDS. Romiplostim is a TPO peptide mimetic, while eltrombopag is a nonpeptide TPO receptor agonist. Initial studies appeared to show the efficacy of romiplostim in MDS-LR as monotherapy [35] or in combination with azacitidine [36], decitabine [37], or lenalidomide in a randomized, placebo-controlled, phase II trial [38]. As with ESAs, response seemed to be correlated with lower baseline TPO levels and fewer platelet transfusions [39]. This led to a randomized, phase II, double-blinded trial of romiplostim compared to placebo, which was terminated prematurely at an interim analysis due to concerns for increased transformation to AML [40]. Although romiplostim appeared to be effective in reducing bleeding and platelet transfusions prior to termination of this study [40], longer-term follow up of this study [41] as well as results from an additional study with romiplostim [42] showed no difference in OS, though there was no change in the risk of progression to AML.