scholarly journals Persistent thrombocytopenia in Dengue Fever is rare but not uncommon - can be treated with steroid successfully

2021 ◽  
Vol 32 (1) ◽  
pp. 62-64
Author(s):  
Md Daharul Islam ◽  
Khaleda Akter ◽  
Ranajit Sen Chowdhury ◽  
Mohammad Abdus Sattar Sarkar ◽  
Aminur Rahman
Keyword(s):  
Platelet Count ◽  
Dengue Fever ◽  
Immune Thrombocytopenia ◽  
Haemorrhagic Fever ◽  
Platelet Destruction ◽  
Immune Mediated ◽  
Immune Injury ◽  
Underlying Mechanisms ◽  
Common Manifestation ◽  
Persistent Thrombocytopenia

Fever, skin rash, thrombocytopenia and bleeding are common manifestation of dengue fever (DF). Thrombocytopenia usually gets better and platelet count normalizes by day 10 of fever. Chronic thrombocytopenia is not a feature of dengue fever. Proposed mechanisms behind thrombocytopenia are many. Direct platelet destruction by dengue virus, immune-mediated platelet destruction and evenmegakaryocytic immune injury are proposed as underlying mechanisms. We are reporting a case of a 43 year old female who presented in dengue season in 2019 with fever and bleeding and wasdiagnosed as a case of dengue haemorrhagic fever. She had persistent thrombocytopenia which neededto be treated on the lines of immune thrombocytopenia and responded to steroids. Other causes of thrombocytopenia were ruled out. Bangladesh J Medicine January 2021; 32(1) : 62-64

scholarly journals Dimethyl fumarate inhibits antibody-induced platelet destruction in immune thrombocytopenia mouse

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Huan Tong ◽  
Yangyang Ding ◽  
Xiang Gui ◽  
Zengtian Sun ◽  
Guozhang Wang ◽  
...  
Keyword(s):  
Platelet Count ◽  
Immune Thrombocytopenia ◽  
Mononuclear Cells ◽  
Dimethyl Fumarate ◽  
Treg Cells ◽  
Antiplatelet Antibody ◽  
Platelet Destruction ◽  
Immune Mediated ◽  
Ifn Γ

Abstract Background Immune thrombocytopenia (ITP) is an autoimmune disease characterized as a low platelet count resulting from immune-mediated platelet destruction. Dimethyl fumarate (DMF) is widely applied for the treatment of several autoimmune diseases with immunosuppressive effect. However, whether it ameliorates ITP is unclear. This study aims to evaluate whether DMF has a preventive effect on ITP in mice. Methods DMF (30, 60 or 90 mg/kg body weight) was intraperitoneally injected into mice followed by injection of rat anti-mouse integrin GPIIb/CD41antibody to induce ITP. Peripheral blood was isolated to measure platelet count and spleen mononuclear cells were extracted to measure Th1 and Treg cells along with detecting the levels of IFN-γ, and TGFβ-1 in plasma and CD68 expression in spleen by immuohistochemical staining. Additionally, macrophage cell line RAW264.7 was cultured and treated with DMF followed by analysis of cell apoptosis and cycle, and the expression of FcγRI, FcγRIIb and FcγRIV mRNA. Results DMF significantly inhibited antiplatelet antibody-induced platelet destruction, decreased Th1 cells and the expression of T-bet and IFN-γ, upregulated Treg cells and the expression of Foxp3 and TGF-β1 as well as reduced CD68 expression in the spleen of ITP mouse. DMF-treated RAW264.7 cells showed S-phase arrest, increased apoptosis and downregulated expression of FcγRI and FcγRIV. Meanwhile, in vitro treatment of DMF also decreased the expression of cyclin D1 and E2, reduced Bcl-2 level and increased Bax expression and caspase-3 activation. Conclusions In conclusion, DMF prevents antibody-mediated platelet destruction in ITP mice possibly through promoting apoptosis, indicating that it might be used as a new approach for the treatment of ITP.

scholarly journals Graft-v-host disease is associated with autoimmune-like thrombocytopenia [see comments]

Blood ◽  
1989 ◽  
Vol 73 (4) ◽  
pp. 1054-1058 ◽  
Author(s):  
C Anasetti ◽  
W Rybka ◽  
KM Sullivan ◽  
M Banaji ◽  
SJ Slichter
Keyword(s):  
Platelet Count ◽  
Marrow Transplantation ◽  
Chronic Gvhd ◽  
Platelet Destruction ◽  
Marrow Graft ◽  
Host Disease ◽  
Antiplatelet Antibodies ◽  
Platelet Survival ◽  
Allogeneic Marrow Transplantation ◽  
Persistent Thrombocytopenia

Abstract Persistent thrombocytopenia after allogeneic marrow transplantation is associated with poor patient survival. To identify the mechanisms of the thrombocytopenia, we studied platelet and fibrinogen kinetics and antiplatelet antibodies in 20 patients between 60 and 649 days (median 90) after transplantation. Seventeen patients had isolated thrombocytopenia (less than 100 X 10(9) platelets/L): the marrow cellularity was normal in five patients and slightly reduced in 12, and there was no discrepancy between thrombopoiesis and myeloerythropoiesis. Three patients had pancytopenia following marrow graft rejection (two) and relapse of leukemia (one). Only three patients had evidence of increased platelet production, indicating that in most cases there is a poor marrow response to thrombocytopenia early after marrow grafting. There was no correlation between platelet count and splenic pooling, suggesting that hypersplenism was an unlikely mechanism of the thrombocytopenia. Although there was a direct relationship between platelet count and platelet survival, the reduction in platelet survival was greater than what could be explained by the fixed platelet removal found in thrombocytopenic patients; this suggests increased platelet destruction. Seven patients had intercurrent infections that reduced both platelet and fibrinogen survivals. In addition, platelet antibodies bound to autologous or marrow donor platelets were present in five of the 12 patients studied. Patients with antiplatelet antibodies had lower platelet counts (30 +/- 10 X 10(9)/L v. 49.1 +/- 28.7 X 10(9)/L, P less than 0.05) and platelet survivals (1.32 +/- 0.92 days v. 3.58 +/- 2.02 days, P less than 0.05) than patients without antiplatelet antibodies. Furthermore, platelet- bound autoantibodies were present in five of six patients with grade II- IV acute or chronic graft-versus-host disease (GVHD), but were not present in six patients free of GVHD (P less than 0.01). We conclude that persistent thrombocytopenia after marrow transplantation is most often secondary to increased platelet destruction mediated by multiple mechanisms and that platelet autoantibodies are found in patients with acute or chronic GVHD.

scholarly journals Diagnosis and Management of Immune Thrombocytopenia in the Era of Thrombopoietin Mimetics

Hematology ◽  
2011 ◽  
Vol 2011 (1) ◽  
pp. 384-390 ◽  
Author(s):  
Howard A. Liebman ◽  
Vinod Pullarkat
Keyword(s):  
Immune Thrombocytopenia ◽  
Randomized Trials ◽  
Current Data ◽  
Disease Course ◽  
Efficacy And Safety ◽  
Platelet Destruction ◽  
Immune Mediated ◽  
Thrombopoietin Receptor ◽  
Diagnostic Work ◽  
Work Up

Abstract The recognition of that patients with Immune Thrombocytopenia (ITP) have functional thrombopoietin deficiency and decreased platelet production due to immune-mediated megakaryocytic injury has challenged the traditional view of this disease as predominantly a disorder of antibody-mediated platelet destruction. The therapy of chronic refractory ITP has been transformed by the approval of the thrombopoietin minetics, romiplostim and eltrombopag, which have shown remarkable efficacy in randomized trials. The use of these agents earlier in the disease course after failure of corticosteroid therapy remains controversial. In this article, we review the current data on the efficacy and safety of thrombopoietin receptor agonists and discuss other therapies as well as diagnostic work up of ITP.

scholarly journals Chronic Immune Thrombocytopenia and Hashimoto’s Hypothyroidism in an Adolescent: Presentation and Implications

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Judy Ibrahim ◽  
Mohammad Alashqar ◽  
Shamma Al Zaabi ◽  
Omar Trad ◽  
Amar Al Shibli
Keyword(s):  
Platelet Count ◽  
Immune Thrombocytopenia ◽  
Adult Population ◽  
Blood Platelet ◽  
Hashimoto Thyroiditis ◽  
Immune Mediated ◽  
Immunosuppressive Medications ◽  
Population Treatment ◽  
Blood Platelet Count ◽  
Chronic Immune Thrombocytopenia

Immune thrombocytopenia (ITP) is a disorder characterized by immune-mediated destruction of thrombocytes leading to peripheral blood platelet count of <100 × 10^9/L. Primary ITP is a terminology used in the absence of other causes or disorders that may be associated with thrombocytopenia, i.e., isolated thrombocytopenia. The term secondary ITP is used if such diseases coexist. We present here a case of a 14-year-old female diagnosed with immune thrombocytopenia. When her evaluation was not strongly supportive of primary ITP, she was screened and proved to have a concomitant Hashimoto thyroiditis. Contrary to the popular belief about secondary ITP in adult population, treatment of our patient’s hypothyroidism did not improve her platelet’s count, and the patient needed multiple immunosuppressive medications to improve her condition.

scholarly journals Rapid response to mycophenolate mofetil in combination with romiplostim in a case of severe refractory immune thrombocytopenia post COVID-19 vaccination

2021 ◽  
Author(s):  
snigdha nutalapati ◽  
gerhard hildebrandt
Keyword(s):  
Platelet Count ◽  
Mycophenolate Mofetil ◽  
Immune Thrombocytopenia ◽  
Rapid Response ◽  
Active Bleeding ◽  
Immune Mediated ◽  
Refractory Itp ◽  
Count Recovery

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.

scholarly journals New Developments in the Pathophysiology and Management of Primary Immune Thrombocytopenia

2020 ◽  
Author(s):  
Karina Althaus ◽  
Christoph Faul ◽  
Tamam Bakchoul
Keyword(s):  
Platelet Count ◽  
Immune Thrombocytopenia ◽  
Clinical Manifestations ◽  
Bleeding Risk ◽  
Platelet Destruction ◽  
New Developments ◽  
Primary Hemostasis ◽  
Current Therapies ◽  
Low Platelet Count ◽  
Bleeding Manifestation

AbstractImmune thrombocytopenia (ITP) is an autoimmune disease that is characterized by a significant reduction in the number of circulating platelets and frequently associated with bleeding. Although the pathogenesis of ITP is still not completely elucidated, it is largely recognized that the low platelet count observed in ITP patients is due to multiple alterations of the immune system leading to increased platelet destruction as well as impaired thrombopoiesis. The clinical manifestations and patients' response to different treatments are very heterogeneous suggesting that ITP is a group of disorders sharing common characteristics, namely, loss of immune tolerance toward platelet (and megakaryocyte) antigens and dysfunctional primary hemostasis. Management of ITP is challenging and requires intensive communication between patients and caregivers. The decision to initiate treatment should be based on the platelet count level, age of the patient, bleeding manifestation, and other factors that influence the bleeding risk in individual patients. In this review, we present recent data on the mechanisms that lead to platelet destruction in ITP with a particular focus on current findings concerning alterations of thrombopoiesis. In addition, we give an insight into the efficacy and safety of current therapies and management of ITP bleeding emergencies.

scholarly journals Graft-v-host disease is associated with autoimmune-like thrombocytopenia [see comments]

Blood ◽  
1989 ◽  
Vol 73 (4) ◽  
pp. 1054-1058
Author(s):  
C Anasetti ◽  
W Rybka ◽  
KM Sullivan ◽  
M Banaji ◽  
SJ Slichter
Keyword(s):  
Platelet Count ◽  
Marrow Transplantation ◽  
Chronic Gvhd ◽  
Platelet Destruction ◽  
Marrow Graft ◽  
Host Disease ◽  
Antiplatelet Antibodies ◽  
Platelet Survival ◽  
Allogeneic Marrow Transplantation ◽  
Persistent Thrombocytopenia

Persistent thrombocytopenia after allogeneic marrow transplantation is associated with poor patient survival. To identify the mechanisms of the thrombocytopenia, we studied platelet and fibrinogen kinetics and antiplatelet antibodies in 20 patients between 60 and 649 days (median 90) after transplantation. Seventeen patients had isolated thrombocytopenia (less than 100 X 10(9) platelets/L): the marrow cellularity was normal in five patients and slightly reduced in 12, and there was no discrepancy between thrombopoiesis and myeloerythropoiesis. Three patients had pancytopenia following marrow graft rejection (two) and relapse of leukemia (one). Only three patients had evidence of increased platelet production, indicating that in most cases there is a poor marrow response to thrombocytopenia early after marrow grafting. There was no correlation between platelet count and splenic pooling, suggesting that hypersplenism was an unlikely mechanism of the thrombocytopenia. Although there was a direct relationship between platelet count and platelet survival, the reduction in platelet survival was greater than what could be explained by the fixed platelet removal found in thrombocytopenic patients; this suggests increased platelet destruction. Seven patients had intercurrent infections that reduced both platelet and fibrinogen survivals. In addition, platelet antibodies bound to autologous or marrow donor platelets were present in five of the 12 patients studied. Patients with antiplatelet antibodies had lower platelet counts (30 +/- 10 X 10(9)/L v. 49.1 +/- 28.7 X 10(9)/L, P less than 0.05) and platelet survivals (1.32 +/- 0.92 days v. 3.58 +/- 2.02 days, P less than 0.05) than patients without antiplatelet antibodies. Furthermore, platelet- bound autoantibodies were present in five of six patients with grade II- IV acute or chronic graft-versus-host disease (GVHD), but were not present in six patients free of GVHD (P less than 0.01). We conclude that persistent thrombocytopenia after marrow transplantation is most often secondary to increased platelet destruction mediated by multiple mechanisms and that platelet autoantibodies are found in patients with acute or chronic GVHD.

scholarly journals Thrombosis in Patients with Immune Thrombocytopenia ,Review of Literature

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 9-10
Author(s):  
Maimoonah Rasheed ◽  
Ashraf Tawfiq Soliman ◽  
Mohamed A Yassin
Keyword(s):  
Platelet Count ◽  
Venous Thrombosis ◽  
Immune Thrombocytopenia ◽  
Thrombotic Event ◽  
Bleeding Tendency ◽  
Accelerated Atherosclerosis ◽  
Immune Mediated ◽  
Increased Risk ◽  
Low Platelet Count ◽  
Active Disease

Introduction ITP is characterized by low platelet count due to immune mediated destruction and bleeding tendency. However, during last few decades thromboembolic events have been reported in patients with ITP. This review is done to study the reported cases of thromboembolic phenomenon in patient with ITP in an attempt to assess the patient characteristics and to understand the underlying mechanism. Methods We searched google Scholar, PubMed about cases with ITP and thrombosis the summary is presented in the following table (Table 1). Results Around 30 reported cases of ITP with thrombotic events were identified and a total of 36 events were recognized in last 10 years. The ages ranged from 3 years to 81 years with a mean of 51 years. Most of the patients were young and middle aged (18-65 years of age), meanwhile around 9 patients were elderly (age &gt; 65 years). Only 3 cases were observed in pediatric age. Almost equal incidence in both genders was recognized. Half of the patient had chronic ITP while in the rest it was diagnosed less than a year. 20 out of 36 (55.6%) events happened at platelet count less than 100*10^9. While 16 events were reported with platelet count higher than this or unknown. Majority of the patients (around 64%) developed arterial events while fewer developed venous thrombosis. For treatment, most of the patients (44%) were not receiving any particular treatment for ITP at the time of thrombotic event. While 6 events (17%) happened while being treated with IVIG and 10 events (28%') happened while on TPO-RA. Only 3 patients were treated with corticosteroids prior to the event. In patients treated with TPO-RAs arterial and venous events were almost similar (57% vs 43% respectively) while majority of the events happened at lower than normal platelet count (7/10 events). Almost half of the patients had one or more underlying risk factor predisposing to atherosclerosis and thrombosis. Most of the patients were treated appropriately for the events with either antiplatelet agents or anticoagulation while simultaneously treatment for ITP was given. Corticosteroids were most frequently used for ITP during the episode followed by IVIG (52% and 28% of total treated patients respectively). Only 1 patient was treated with TPO-RA after the event for low platelet counts while others received other treatments (Rituximab, Danazol and splenectomy). Discussion Thrombosis is a complex process involving arteries and veins. Accelerated atherosclerosis and plaque rupture is the underlying event for arterial thrombosis. While in venous thrombosis immobility and procoagulant states are the main factors. Immune thrombocytopenia is characterized by immune mediated destruction and impaired production of platelets predisposing to bleeding mostly. However, it is a unique pathological process that is linked to both bleeding and thrombosis. Multiple factors predispose patients to thrombosis in ITP. The patients with chronic and active disease are particularly at risk of paradoxical thrombosis due to accelerated atherosclerosis as in other autoimmune conditions, predisposing to arterial thrombotic events. Active disease is also characterized by increased turnover of platelets in bone marrow and higher levels of circulating platelets microparticles (PMPs) which promote thrombin formation and promote venous thrombosis. The patients treated with IVIG and TPO-RA are at higher risk as compared to other forms of treatment. IVIG is used in acute states as it prevents the destruction of platelets but simultaneously promotes thrombosis by increasing blood viscosity and thrombin production. TPO-RAs are agents which mimic the action of thrombopoietin on megakaryocytes promoting their growth and differentiation and increasing platelet production. Increasing platelet count above the normal target might contribute to thrombosis however megakaryocyte activation itself leads to increased risk of thrombosis, despite low platelet count. In patients with ITP and thrombotic events, judicious use of antiplatelet therapy and anticoagulation is indicated along with simultaneous therapy directed at improving platelet count. Conclusion Patient with active ITP are predisposed to thrombosis in addition to bleeding. A treating physician needs to be vigilant to diagnose early the events and then to institute proper use of antiplatelets and anticoagulation along with therapy directed at ITP. Figure Disclosures No relevant conflicts of interest to declare.

scholarly journals Eltrombopag-based combination treatment for immune thrombocytopenia

2018 ◽  
Vol 9 (10) ◽  
pp. 309-317 ◽  
Author(s):  
David Gómez-Almaguer
Keyword(s):  
Platelet Count ◽  
Immune Thrombocytopenia ◽  
Critical Role ◽  
Physiological Mechanism ◽  
Newly Diagnosed ◽  
Platelet Destruction ◽  
Simultaneous Treatment ◽  
Platelet Production ◽  
Thrombopoietin Receptor ◽  
Lymphocyte Activity

Immune thrombocytopenia (ITP) is a bleeding disorder caused by a decrease in platelet count resulting from increased destruction and insufficient production of platelets. Although impaired regulatory T-lymphocyte activity plays a critical role in platelet destruction, many other immunologic abnormalities are also likely to be involved. Importantly, patients with ITP appear to have defects in a thrombopoietin-mediated physiological mechanism that compensates for a decrease in platelet count by increasing platelet production. Thus, simultaneous treatment of multiple pathogenic pathways involved in ITP could potentially result in synergistic efficacy. While conventional treatments for ITP suppress or modulate the immune system to reduce platelet destruction, a unique class of ITP therapy, namely thrombopoietin receptor agonists (TPO-RAs), improves platelet production by activating the thrombopoietin pathway. As hypothesized, preliminary studies show that combinations of eltrombopag, an oral TPO-RA, with conventional treatments improve outcomes in both newly diagnosed and refractory patients. In this review, the clinical experience with eltrombopag-based combinations in patients with ITP is summarized and the implications of the available data are discussed.

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