Secondary Immune Thrombocytopenic Purpura Research Articles

Ayurveda’s Role in Managing ITP: A Case Study

ITP (Immune thrombocytopenic purpura) is an autoimmune disorder where the immune system mistakenly attacks the platelets leading to the low platelet levels. ITP may occur in the absence of a predisposing cause (primary ITP) or due to a growing list of associated conditions (secondary ITP), and must be differentiated from other causes of thrombocytopenia. ITP can be acute and chronic. It can cause purple bruises and tiny purple red dots on the skin that looks like a rash. Modern medicine has no effective treatment for ITP. A 26 year old female patient presented with the complaints of bruises, nose bleeding, heavy menstruation, pain in left leg and irritability. The clinical findings and symptoms of the patient pointed to ITP. It is associated with Tiryagata Raktapitta in Ayurvedic diagnosis. The patient was given Platoplan along with Kumar Kalyan Ras, Swarn Vasant Malti Ras, Pitta Balance. After a month, the patient reported relief in some of the symptoms. Platelet count increased from 41,000 to 1,89,000. After completing the medications the most common problem of low platelets reduced.

Primary Immune Thrombocytopenic Purpura (ITP) and ITP Associated with Systemic Lupus Erythematosus: A Review of Clinical Characteristics and Treatment Modalities.

Immune thrombocytopenic purpura (ITP) is an immune-mediated disorder characterized by the destruction of platelets and megakaryocytes due to autoantibodies against the platelet surface proteins. ITP without any apparent cause of thrombocytopenia is defined as primary ITP, and ITP in the setting of SLE is secondary ITP, which can be diagnosed after excluding other causes of thrombocytopenia by history, physical examination, and laboratory testing. Patients with ITP associated with SLE have higher median platelet count and less bleeding manifestations compared to the patients with primary ITP. It can be very challenging to diagnose primary ITP in SLE patients as other causes of thrombocytopenia including drug-induced thrombocytopenia, antiphospholipid syndrome, and thrombotic microangiopathic process should be ruled out. Corticosteroids are the main modality of treatment. IVIG can be used in severe cases. Splenectomy was found to be less effective in ITP associated with SLE compared to primary ITP. Control of disease activity with immunosuppressive therapy can be helpful in some cases associated with active disease flares in SLE patients.

Immune thrombocytopenic purpura following mRNA-SARS-CoV-2 vaccination: a case report

Introduction: Herein, it is presented a case report of a Colombian adult male patient, without any previous report of thrombocytopenia or hematological disorders, who developed a mild and chronic paucisymptomatic immune thrombocytopenic purpura, a rare complication following SARS-CoV-2 m-RNA. To the best of our knowledge, this represents the first documented case in Colombia of immune thrombocytopenic purpura associated with mRNA vaccines (BNT162b2 or mRNA-1273), with a comprehensive 2-year clinical follow-up. Case Description: The patient received the initial and second doses of the mRNA BNT162b2 vaccine in June 2021, the first booster dose in November 2021 (mRNA-1273), and the second booster dose (mRNA BNT162b2) in June 2022. Thrombocytopenia (<100 x109 platelets/L, which is the criterion to define immune thrombocytopenic purpura) was documented after the second vaccination dose and both boosters, and it improved after corticosteroid therapy. However, cycling thrombocytopenia persisted until the clinical follow-up in August 2023, with platelet count ranging from 57 to 191 x109 platelets/L (mean: 103 x109 platelets/L). Conclusion: Given that secondary immune thrombocytopenic purpura can occur following SARS-CoV-2 mRNA vaccination, systematic research to identify risk factors associated with immune thrombocytopenic purpura due to COVID-19 immunization should be conducted.

A case of secondary immune thrombocytopenia induced by atezolizumab plus bevacizumab therapy for hepatocellular carcinoma resulting in death from intracranial hemorrhage

An 84-year-old woman underwent laparoscopic partial hepatectomy for a single 3.0-cm-diameter nodule of hepatocellular carcinoma at segment 5. Although the postoperative condition was uneventful, multiple recurrences were observed six months after hepatic resection. Transcatheter arterial chemoembolization (TACE) was the second-line therapy. However, she was later diagnosed as TACE refractory due to residual tumor and presence of portal vein tumor thrombus. Third-line therapy was the combination of atezolizumab and bevacizumab, which was discontinued after 22 courses due to disease progression. Two months after the conclusion of chemotherapy, sudden onset of purpura was observed around her eyes and on her lower legs. Laboratory tests revealed severe thrombocytopenia, and she was diagnosed with secondary immune thrombocytopenic purpura. Steroids and immunoglobulin therapy were then administered. Although the immature platelet fraction increased after treatment, the platelet count did not. The patient died of intracranial hemorrhage 10 days after initiation of steroid and immunoglobulin therapy.

Mortality and Comorbidities of Covid-19 Patients with Immune Thrombocytopenic Purpura - a Review of the National Database 2019-2020

Introduction: Immune thrombocytopenic purpura (ITP) is a diagnosis of exclusion that is characterized by isolated thrombocytopenia with a generalized purpuric rash. If there is a known case for the ITP, it is referred to as secondary ITP. Secondary ITP may often be caused by drugs, systemic immunologic, or infectious diseases. Covid-19 is a disease caused by the SARS-CoV-2 virus, which caused a pandemic in 2020, affecting hundreds of millions of people worldwide. There have been several different hematologic conditions associated with this viral infection, including deep vein thromboses, pulmonary emboli, and many patients with ITP induced by Covid-19. With several case reports and case series available on these patients, the specifics behind the strength of the association, mortality of the patients, and their comorbidities have not been previously explored. Methods: Using the national inpatient sample from the years 2019-2020, we analyzed adult hospitalized patients with ITP and Covid-19 based on their International Classification of Diseases - 10 clinical modification codes. We calculated the odds ratios for patients with Covid-19 being diagnosed with ITP compared to other hospitalized patients. Additionally, we calculated the odds of several complications, treatments, as well as concurrent conditions in patients with Covid-19 and ITP. The complications measured were epistaxis or hemoptysis, intracranial hemorrhage (ICH), non-intracranial hemorrhage (nICH), deep vein thrombosis (DVT), pulmonary embolism (PE), and death. Treatments measured were transfusion with either red blood cells (RBC) or platelets. The concurrent conditions evaluated were systemic lupus erythematosus (SLE), hepatitis C and heparin-induced thrombocytopenia (HIT). Results Out of the 115,150 hospitalized patients with ITP included in the database, 0.02% of them were diagnosed with Covid-19. The odds of a patient with Covid-19 being diagnosed with ITP were lower than those for other hospitalized patients (OR=0.860 [0.787-0.941], p=0.001). The mean age for patients with ITP diagnosed with Covid-19 was 64.1 compared to 60.9 in patients without Covid-19 (p=0.001). Hospitalized patients with ITP who were also diagnosed with Covid-19 were at a higher risk of developing epistaxis (OR: 1.45 [1.01-2.07], p=0.042), pulmonary embolism (OR: 2.22 [1.35-3.66], p=0.002), and death (OR: 4.39 [3.33-5.80], p<0.001) compared to those without Covid-19. They were not at higher odds of developing a DVT (OR: 1.25 [0.798-1.97], p=0.325), ICH (OR: 0.158 [0.0160-1.56], 0.114) or nICH (OR: 1.03 [0.678-1.55], p=0.905). They were not significantly more or less likely to get transfused with RBC (OR: 0.816 [0.585-1.14], p=0.231) or platelets (OR: 1.14 [0.865-1.53], p=0.337). The ITP patients with concurrent Covid-19 were also not more likely to suffer from SLE (OR: 0.737 [0.453-1.20], p= 0.222), Hepatitis C (OR: 0.760 [0.392-1.47], 0.416), or HIT (OR: 1.16 [0.181-7.49], p=0.872). Conclusion Hospitalized patients with Covid-19 were at a lower risk of being diagnosed with concurrent ITP than other hospitalized Covid-19 patients. Those with ITP who also had Covid 19 had significantly higher odds of complication of bleeding with epistaxis or hemoptysis as well as a higher risk of pulmonary embolism and death. However, they were not at higher risk of hemorrhage elsewhere or DVT. They were not treated with transfusions differently and having SLE, hepatitis C or HIT did not place hospitalized patients with ITP at a higher risk of developing Covid-19.

Immune Thrombocytopenic Purpura and Paradoxical Thrombosis: A Systematic Review of Case Reports.

Immune thrombocytopenic purpura (ITP) is an acquired bleeding disorder characterized by autoantibodies against platelets. The clinical presentation is variable; the main symptom is bleeding, and many patients are asymptomatic; others have nonspecific symptoms like fatigue. Uncommonly, ITP can present with paradoxical thrombosis. The risk of thrombosis in ITP may be higher than expected, which makes the management of ITP more challenging. This review aims toevaluate patients with ITP who develop thrombosis and identify potential risk factors related to thrombosis in this category of patients. English literature was searched using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines for adults above 18 years with primary ITP who had infarctions or thrombotic events. PatientswithsecondaryITP were excluded. The search included articles published up to 20th October 2021. A total of73 articles were included. Seventy-seven patients with ITP had developed infarctions and various thrombotic events.Sixty-three patients had arterialevents, and 14 patients developed venous thrombotic events. Patients with ITP have low platelets, which predispose them to bleed; despite that, serious thrombotic complications can happen in these patients and are difficult to predict. Therefore, it is critical for physicians to understand that ITP is paradoxically a prothrombotic condition and to address preventive thromboembolic measures whenever possible.

Cardiovascular and Hematologic Complications of COVID-19 Vaccines.

COVID-19 is a prothrombotic and cardiac-damaging disease. There are 4 vaccines against COVID-19 currently approved in North America, including the mRNA vaccines by Pfizer and Moderna, and the adenovirus vector vaccines by Johnson and Johnson and AstraZeneca. These vaccines have been proven effective in reducing morbidity and preventing mortality in patients who were exposed to COVID-19 infection, but the vaccines have also been associated with complications. Vaccine-induced thrombotic thrombocytopenia (VITT) has a similar pathogenesis to heparin-induced thrombocytopenia, with an inappropriate immune response leading to platelet activation, consumption of platelets, and thrombosis. It appears to be more common with the adenovirus vector vaccines. Secondary immune thrombocytopenic purpura has been reported with all COVID-19 vaccines and is distinct from VITT because there is no sign of platelet activation or thrombotic events. Myocarditis and pericarditis are often reported in young males following mRNA vaccines and is often associated with a full recovery. The long-term effects of VITT, secondary immune thrombocytopenic purpura, myocarditis, and pericarditis secondary to COVID-19 vaccines have yet to be elucidated. Continued surveillance for these complications after vaccination is crucial for accurate diagnosis and effective management. Patients should consult their physicians regarding repeated vaccine doses after experiencing an adverse effect.

An Unusual Cause of Secondary ITP in a 34-Year-Old Hispanic Male

Secondary immune thrombocytopenic purpura (ITP) associated with Helicobacter pylori (H. pylori) infection has been described in the literature. It appears to have a geographic distribution; mostly encountered in countries with a higher prevalence for H. pylori such as Italy or Japan. H. pylori eradication has been recommended in the management of ITP with studies showing improvement in the platelet count in some patients. Substantial platelet count increases in patients with severe thrombocytopenia (platelet counts <30 × 103 microliter), however, are uncommon with H. pylori treatment alone. Here, we present a 34-year-old Hispanic male with worsening chronic thrombocytopenia that resolved following eradication of his H. pylori infection. Herein, we highlight a rare and reversible cause of secondary ITP. With this case report, we hope to encourage physicians to include H. pylori testing in the evaluation of thrombocytopenia.

Mixed connective tissue disease with secondary immune thrombocytopenic purpura -- a case report

The Journal of the Postgraduate Institute of Medicine (JPGIM) is an open access, peer-reviewed, biannual journal published by the Postgraduate Institute of Medicine (PGIM) of the University of Colombo (UOC), Sri Lanka. The JPGIM aims to publish articles relevant to clinicians, policymakers, and researchers on topics relating to the practice of medicine, medical education, professionalism, integrity, and ethics of the research enterprise. The JPGIM has been in publication since 2014 and publishes accepted manuscripts online immediately after copy-editing, enabling rapid dissemination of scientific knowledge. The published articles are compiled into two issues in June and December.The Journal practices a double-blind peer review policy. The JPIGM does not charge any article processing or publication fee.We recommend that you review the About the Journal page for the journal's section policies, as well as the Submission Guidelines. Authors need to register with the journal prior to submitting or, if already registered, can simply log in and begin the five-step process.

Efficacy and Safety of Biosimilar Romiplostim in Immune Thrombocytopenic Purpura : Single Centre Retrospective Data Analysis

Introduction: Thrombopoietin receptor agonist (TPO RA) is an approved second line of treatment in Persistent and Chronic Immune Thrombocytopenic Purpura (ITP).However in India due to cost constraints, the majority prefer Immunosuppression therapy. A biosimilar of Romiplostim (Romy®) is developed and launched in India, by Intas Pharmaceuticals, India, in July 2019, its monthly cost is around $160, a huge relief to ITP patients (pts), now accessible to the masses in Lower Middle Income Country (LMIC), India. Real-world experience data on Romiplostim (Romy®) in ITP is sparse. Aim: A single centre retrospective data analysis to evaluate the Safety and Efficacy of Biosimilar Romiplostim (Romy®) in patients of Immune Thrombocytopenic Purpura. Method: A total of 54 steroid-refractory or steroid-dependent ITP pts were registered at Haemato-oncology Care Centre Vadodara from July 2019 to January 2020, who received Injection Romiplostim (Romy®) treatment. Pre-treatment Complete Blood Count(CBC) Platelet count (PLT) ,Liver Function Test ,Renal Function Tests ,PT,PTT,ANA,HIV,HBsAg,HCV,Bone Marrow,USG Abdomen, Chest X-Ray was done.All patients had pretreatment Platelet count less than 30000/cumm.The dose of Romiplostim was 1mcg /kg to 6 mcg/kg, subcutaneous once a week.12 /54 patients who had active bleeding also received concomitant Rituximab 100mg IV infusion once a week for 4 weeks. The response was assessed by CBC PLT every week for the first 4 weeks, later on, every monthly. The response was labelled as Optimum if PLT count maintained between 50000/cumm to 4,00,000/cumm, Suboptimal if PLT count increased from baseline but remained below 50,000/cumm, No response if no increment from baseline PLT count. Romiplostim was continued with the same dose if response was Optimum, escalated if response was Suboptimal, de-escalated if PLT increased above 1, 50,000/cumm and stopped if PLT increased above 4,00,000/cumm or no response found after 4 weeks of treatment. Results: Atotal of 54 pts were evaluated, 23(42%) Male, 31(58%) Female, Median age 40 years (range 8 yrs to 85yrs).Persistent ITP was the diagnosis in 38/54(70%)pts, Chronic ITP in 16/54(30%) pts, Secondary ITP in 17(30%) pts, with 14 patients had ANA positive, 2 patients had HCV positive, 1 patient had tubercular lymphadenopathy. The overall response rate (ORR) was 50/54(93%).Optimum response in 49 /54 (91%),Suboptimal response in 1/54 (2%),No response in 4/54(7%)pts. ORR in patients who received Rituximab with Romiplostim was 12/12 (100%). Time to achieve response was 1 week in 46 (85%) pts, 2 weeks in 3(5%) pts, and 3 weeks in 1 (2%) pts. Follow up assessment showed a total of 21/54 (40%) patients had sustained optimum response for more than 6 months with continuation of once a week Romiplostim,9/54 (16%) had sustained response for more than 6 months even on discontinuation of Romiplostim after 4 weeks.8/54(15%) pts with ANA positive reports required a combination of immunosuppressant with Romiplostim to maintain prolonged sustained response.4/54(7%) pts did not respond to Romiplostim hence it was stopped after 4 weeks. Mild adverse effects were observed headache 5(9%), myalgia 3 (5%), bone pains 6(11) Abdominal pain 4(7%) pts. Romiplostim was stopped in 12 (22%) pts because of thrombocytosis (PLT above 4, 50,000/cumm) after a first single dose of Romiplostim. None of the patients had serious adverse events Conclusion: Biosimilar Romiplostim, (Romy®) has shown rapid, excellent and sustained response in the majority of ITP pts in our study. Its affordable cost fulfils an unmet need of ITP patients, requiring the best second line of treatment in LMIC Disclosures No relevant conflicts of interest to declare.

Laboratory Tests Used in the Diagnosis of Immune Thrombocytopenia and General Treatment Approaches

Immune thrombocytopenia currently called under its’ new name, immune thrombocytopenic purpura (ITP) is a disease characterized by thrombocytopenia, in which the body attacks its own platelets due to the disorders in immune system. The pathophysiology of this disease includes increased platelet destruction and most megakaryocyte production in bone marrow. The most common clinical manifestation of ITP is mild or severe progressive bleeding that could result in death. ITP is generally named as primary or secondary ITP according to thrombocytopenia severity, disease duration, bleeding status and secondary occurrence of the disease. Currently for diagnosis, despite the blood count, antiglobulin test and laboratory tests that can detect platelet-bound antibodies, they are not enough for definitive diagnosis. Like the difficulty in diagnosis, ITP treatment is quite complicated which varies depending on age, characteristics and risk of the patient. It is classified as first, second and third-line treatment options. Also, depending on the condition of patients, combined treatment might be an option which increases the complexity of the treatment. Unfortunately, discussions related to different clinical applications in diagnosis and treatments continue recently. For this reason, we considered that preparation of a review containing recent updates in diagnostic approaches and treatment options in ITP will be remarkable and beneficial for physicians interested in this subject.

Immune thrombocytopenic purpura increased risk of subsequent pancreatitis: A Nationwide population cohort study

Immune thrombocytopenic purpura (ITP) is characterized by thrombocytopenia and bleeding diathesis. Pancreatitis is a very rare complication but may be fatal. We analyzed data of newly diagnosed ITP patients, excluding those with a history of splenectomy, unknown sex or date of birth, or preexisting pancreatitis at the time of ITP diagnosis, and compared these with selected age-, gender-, and index-year-matched controls, using the Taiwan National Health Insurance Research Database from 1996 to 2013. The study enrolled 100,177 ITP patients and 100,177 controls. We found that pancreatitis risk was higher in secondary ITP patients, regardless of age group, gender, baseline Charlson comorbidity index (CCI) score, history of biliary stone, hyperlipidemia, or alcoholism, than in the control population. Primary ITP patients with CCI score 1 and without biliary tract stone history also showed a higher pancreatitis risk than the controls. The incidence rate and cumulative incidence of pancreatitis were increased in primary, secondary, and unspecified ITP cases. These phenomena may be related to the presence of autoantibodies against glycoprotein IIb/IIIa, or to IgG4, microparticle obstruction, or sclerosis. We noted a direct association between ITP and the development of pancreatitis in Taiwan population.

Secondary immune thrombocytopenic purpura with renal cell carcinoma

IntroductionSeveral types of cancers are reported to induce secondary immune thrombocytopenia resembling immune thrombocytopenic purpura‐like syndrome. However, renal cell carcinoma‐induced immune thrombocytopenic purpura is an extremely rare phenomenon.Case presentationA 73‐year‐old male with right renal tumor and multiple enlarged lymph nodes presented severe thrombocytopenia, without bone or hepatic metastasis. Although platelet transfusion and high‐dose immunoglobulin treatment were refractory, surgical resection of the tumor and lymph nodes promptly improved thrombocytopenia. After recurrence, he presented thrombocytopenia again. Tyrosine kinase inhibitor treatment was ceased due to uncontrollable hemorrhagic gastric ulcer. The patient eventually died of cancer 4 months after surgery. Flow cytometry analysis revealed the presence of integrin glycoprotein IIb/IIIa, which is a fibronectin/fibrinogen receptor on platelets and as an antigen in immune thrombocytopenic purpura.ConclusionTo the best of our knowledge, this is the first reported case of renal cell carcinoma‐induced immune thrombocytopenic purpura that demonstrates the presence of platelet‐autoantibody glycoprotein IIb/IIIa.

Immune Thrombocytopenic Purpura Secondary to Varicella Zoster Infection: A Case Report

Varicella zoster infection is usually considered to be benign despite of serious complications. Immune Thrombocytopenic Purpura (ITP) is usually a self-limiting disorder in children. ITP is an autoimmune disorder in which antibody-coated or immune complex–coated platelets are destroyed prematurely by the reticuloendothelial system, resulting in peripheral thrombocytopenia. In primary ITP the thrombocytopenia is isolated, whereas in secondary ITP the condition is associated with other disorders (e.g. Systemic Lupus Erythematous, HIV, VZV). We describe a case of immune Thrombocytopenic Purpura secondary to varicella infection in a previously healthy 7-y-old boy. He was treated successfully with intravenous immunoglobulin (IVIG).

An Unusual Endoscopic Finding: “Polka Dot Stomach”

A 57-year-old woman with no significant past medical history presented to the emergency department with 2 days of melena, epistaxis, purpura, fatigue, and malaise. She endorsed taking sulfamethoxazole/trimethoprim (TMP/SMX) for a sinus infection for 8 days prior to admission. She denied any prior GI bleeding and had a normal screening colonoscopy 6 years prior. She had rare NSAID use and no other medication use. Physical exam revealed purpura on the hard and soft palate, buccal mucosa, and tongue (Figure 1). Petechiae were present on the bilateral lower extremities (Figure 2). Her initial laboratory results revealed severe anemia, hemoglobin (Hgb) of 5.2 g/dL, and severe thrombocytopenia, platelets of 2 K/uL. The Hgb had decreased from 13 g/dL to 5.2 g/dL over 1 day, and platelets had decreased from 199 K/uL to 2 K/uL over 1 week. Her WBC, blood chemistry, coagulation studies, and liver function tests were unremarkable. She received 2 units of packed RBCs, raising the Hgb to 7.7 g/dL and 6 units of platelets. She received upper endoscopy to help determine the etiology of the melena. This showed diffuse gastric petechiae with oozing as the source of the bleed (Figure 3). Based on these findings, immune thrombocytopenic purpura (ITP) or drug-induced immune thrombocytopenia (DITP) leading to upper GI bleeding was the likely diagnosis. The patient was started on IV methylprednisolone and IVIG. Further laboratory studies for HIV, HCV, and other autoimmune serology were negative, excluding secondary ITP. ITP and DITP are similar in that both involve the autoimmune destruction of platelets; however, ITP has no known trigger, whereas DITP is triggered by a drug. TMP/SMX is among a list of drugs known to cause platelet-reactive antibodies. In the acute setting, ITP cannot be distinguished from DITP. As such, steroids, IVIG, and platelet transfusions were started for treatment because of the clinical severity of GI bleeding. The suspected culprit drug was discontinued. The patient's anemia and thrombocytopenia improved over the next several days with the course of IV steroids and IVIG, and she was discharged on an oral steroid taper. Her Hgb and platelets were normal by one-month follow-up. The endoscopic findings of bleeding from ITP or DITP are very rare with only a few case reports to our knowledge. The characteristic stomach petechiae causing a “polka dot” appearance should be noted in patients with ITP or DITP and severely low platelets.Figure 1Figure 2Figure 3

The effect of antiviral therapy on hepatitis C virus-related thrombocytopenia: a case report

BackgroundAutoimmune thrombocytopenic purpura is an immunological disorder characterized by increased platelet destruction due to presence of anti-platelet autoantibodies. Hepatitis C virus infection, which is one of the most common chronic viral infections worldwide, may cause secondary chronic immune thrombocytopenic purpura.Case presentationWe report a case of a 51-year-old Caucasian female with hepatitis C virus infection who developed a severe, reversible, immune thrombocytopenia. Platelet count was as low as 56.000/mm3, hepatitis C virus serology was positive, serum glutamic oxaloacetic transaminase, serum glutamic pyruvic transaminase and gamma-glutamyltransferase serum levels were elevated. Disorders potentially associated with autoimmune thrombocytopenic purpura were ruled out. A corticosteroid treatment was started and led to an increase in platelet count. The patient was then treated with pegylated-interferon alpha 2a and ribavirin. After four weeks of treatment hepatitis C virus - ribonucleic acid became undetectable and steroid treatment was discontinued. Six months of antiviral therapy achieved a sustained biochemical and virological response together with persistence of normal platelet count.ConclusionIn our case report hepatitis C virus seemed to play a pathogenic role in autoimmune thrombocytopenic purpura. Moreover, the successful response (negative hepatitis C virus - ribonucleic acid) to tapered steroids and antiviral therapy was useful to revert thrombocytopenia.

RETRACTED: &amp;lt;i&amp;gt;Aspects of Viral Involvement in Chronic Immune Thrombocytopenic Purpura&amp;lt;/i&amp;gt;

The immune chronic thrombocytopenic purpura is an illness characterized by peripheral thrombocytopenia occurred through a mechanism of early hyper destruction of blood platelets or by deficient platelet synthesis in the medulla. The chronic immune purpura can be primary, autoimmune in nature, thrombocytopenic idiopathic or secondary in the context of other associated pathologies. The idiopathic thrombocytopenic purpura (P.T.I.) is an immune-mediated acquired disorder. It is characterized by isolated thrombocytopenia, defined as platelet count assessment from peripheral blood smear of less than 100.000/mm³, in the absence of a different cause of thrombocytopenia. The secondary immune isolated thrombocytopenia occurs in the context of some associated pathologies. The aim of the study is to highlight the involvement of some infectious agents in the etiopathogenesis of the secondary immune thrombocytopenic purpura. The immune thrombocytopenia can be subordinated to some chronic infections such as infection with virus B or C, infection with virus HIV, infection with Cytomegalovirus (CMV) or the Helicobacter Phylori infection. The study was conducted on a group of 40 patients, distributed into two groups: the first group of patients is the asymptomatic patients who do their common tests while the other group of patients is with bleeding symptoms: Petequiae, bruising, epistaxis, gum bleedings. The studied group puts into evidence a thrombocytopenia with a mean platelet count of 60.20 ± 19.75 × 103/μL. 80% of patients had positive anti-platelet antibodies. Out of these, 20% carry infections with virus B and C while 30% carry Cytometalovirus infection (CMV). The study found one case of HIV infection. Thus we highlight the involvement of infectious agents in the etipathogenesis of secondary immune thrombocytopenic purpura as well as the way they affect the platelet function.

Pathogenesis in immune thrombocytopenia: new insights.

Idiopathic (immune) thrombocytopenic purpura (ITP) is a common autoimmune disorder resulting in isolated thrombocytopenia. ITP can present either alone (primary) or in the setting of other conditions (secondary) such as infections or altered immune states. ITP is associated with a loss of tolerance to platelet antigens and a phenotype of accelerated platelet destruction and impaired platelet production. Although the etiology of ITP remains unknown, complex dysregulation of the immune system is observed in ITP patients. Antiplatelet antibodies mediate accelerated clearance from the circulation in large part via the reticuloendothelial (monocytic phagocytic) system. In addition, cellular immunity is perturbed and T-cell and cytokine profiles are significantly shifted toward a type 1 and Th17 proinflammatory immune response. Further clues into immune dysregulation in ITP may be gleaned from studies of secondary ITP. Some infections can induce antiplatelet Abs by molecular mimicry, and there may be common elements involved in breaking tolerance with other autoimmune disorders. There is also evidence for a genetic predisposition to both ITP and responsiveness to therapy, which may in part lie within immune-related genes. Lastly, treatment with immunomodulatory agents remains the mainstay of ITP therapies.

Pathogenesis in immune thrombocytopenia: new insights

AbstractIdiopathic (immune) thrombocytopenic purpura (ITP) is a common autoimmune disorder resulting in isolated thrombocytopenia. ITP can present either alone (primary) or in the setting of other conditions (secondary) such as infections or altered immune states. ITP is associated with a loss of tolerance to platelet antigens and a phenotype of accelerated platelet destruction and impaired platelet production. Although the etiology of ITP remains unknown, complex dysregulation of the immune system is observed in ITP patients. Antiplatelet antibodies mediate accelerated clearance from the circulation in large part via the reticuloendothelial (monocytic phagocytic) system. In addition, cellular immunity is perturbed and T-cell and cytokine profiles are significantly shifted toward a type 1 and Th17 proinflammatory immune response. Further clues into immune dysregulation in ITP may be gleaned from studies of secondary ITP. Some infections can induce antiplatelet Abs by molecular mimicry, and there may be common elements involved in breaking tolerance with other autoimmune disorders. There is also evidence for a genetic predisposition to both ITP and responsiveness to therapy, which may in part lie within immune-related genes. Lastly, treatment with immunomodulatory agents remains the mainstay of ITP therapies.

Adult Primary and Secondary Immune Thrombocytopenic Purpura

This study was conducted to compare the platelet count and the presence of bleeding manifestations at initial diagnosis of immune thrombocytopenic purpura (ITP) between patients with primary and secondary ITP. Medical records for 67 consecutive adult patients with ITP were reviewed retrospectively and the relevant data were abstracted. Thirty-eight (56.7%) patients were diagnosed as having primary ITP and 29 (43.3%) were considered to have secondary ITP. At the time of diagnosis, the median initial platelet count (median: 60 × 10(9)/L) for patients with secondary ITP was significantly (P < .005) higher than that for patients with primary ITP (median: 3.5 × 10(9)/L). Ecchymosis and/or purpura was observed in 4 (13.8%) patients with secondary ITP and in 33 (86.6%) patients with primary ITP (P value <.005). In conclusion, patients with secondary ITP had higher platelet count at diagnosis and were less likely to present with bleeding manifestations than those with primary ITP.