Background

Immune Thrombocytopenia (ITP), formerly known as Idiopathic Thrombocytopenic Purpura, is an autoimmune disorder that affects the blood. The condition is characterized by a low platelet count in the blood, which can lead to an increased risk of bleeding. Platelets are small cell fragments in the blood that help with clotting. In ITP, the immune system mistakenly targets and destroys platelets, reducing their number in the bloodstream.

The exact cause of ITP is often unknown, hence the term “idiopathic.” The most common symptoms are easy bruising and prolonged bleeding. Petechiae (small, red, or purple spots on the skin), nosebleeds, and bleeding gums are also common. In severe cases, internal bleeding may occur. Diagnosis is based on a thorough medical history, physical examination, blood tests (complete blood count or CBC), and sometimes a bone marrow examination to rule out other potential causes of low platelet count.

The treatment approach depends on the severity of symptoms. In mild cases, observation may be sufficient, and no specific treatment may be required. For more severe cases or those with significant bleeding, treatment options may include corticosteroids, intravenous immunoglobulin (IVIG), immunosuppressive drugs, or, in some cases, splenectomy (removal of the spleen). 

Epidemiology

The epidemiology of Immune Thrombocytopenia (ITP) involves the study of the incidence, prevalence, and distribution of the disease in populations.  

Incidence and Prevalence: 

• ITP can occur at any age but is more common in children and adults under 40 years old. 
• In children, ITP often follows a viral infection and is frequently acute and self-limiting. 
• In adults, ITP can be acute or chronic, with chronic cases more commonly diagnosed in older individuals. 
• The overall incidence of ITP is estimated to be around 3.3 cases per 100,000 person-years. 

Age and Gender Distribution: 

• Childhood ITP often occurs between the ages of 2 and 10 years. 
• Adults can develop ITP at any age, but it is most frequently diagnosed in individuals between 20 and 50 years old. 
• There is a slightly higher incidence in females compared to males. 

Secondary ITP: 

• ITP can be primary (idiopathic), meaning there is no known cause, or secondary to other conditions such as autoimmune disorders, infections, or certain medications. 
• Secondary ITP may have a different epidemiological profile depending on the underlying cause. 

Geographical and Ethnic Variations: 

• The incidence of ITP may vary geographically, and there might be differences in prevalence among different ethnic groups. 
• Some studies suggest a higher incidence in Western countries compared to Asian populations. 

Anatomy

Pathophysiology

The pathophysiology of immune thrombocytopenia (ITP) involves an immune-mediated destruction of platelets, which leads to a decreased platelet count in the bloodstream.  

Autoimmune Response: 

• ITP is considered an autoimmune disorder, meaning the body’s immune system mistakenly attacks its cells. In this case, platelets are the target. 
• The immune system produces antibodies (specifically, anti-platelet antibodies) that recognize platelets as foreign and tag them for destruction. 

Platelet Destruction:  

• Antibodies bind to the surface of platelets, marking them for destruction by the spleen and other macrophages in the reticuloendothelial system. 
• The spleen plays a central role in the destruction of antibody-coated platelets. The antibodies facilitate the binding of platelets to the Fc receptors on macrophages, promoting their removal from circulation. 

Suppression of Platelet Production: 

• In addition to increased platelet destruction, there may be a suppression of platelet production in the bone marrow. 
• It is believed that immune mechanisms, including cytokines and T cells, contribute to the inhibition of platelet production. 

Role of T Cells: 

• T lymphocytes, a type of white blood cell, play a role in the pathogenesis of ITP. They may activate B cells to produce anti-platelet antibodies and directly target platelets for destruction. 

Presence of Anti-Platelet Antibodies: 

• A characteristic feature of ITP is the detection of anti-platelet antibodies, particularly anti-glycoprotein IIb/IIIa and anti-glycoprotein Ib/IX antibodies. 
• These antibodies can be identified in the blood of individuals with ITP, supporting the autoimmune nature of the disorder. 

Secondary ITP: In some cases, ITP may be secondary to other conditions such as infections, autoimmune diseases, or malignancies. In secondary ITP, the underlying condition contributes to immune dysregulation and platelet destruction. 

Genetic Factors: While most cases of ITP are idiopathic, some genetic factors may contribute to an individual’s susceptibility to developing the disorder. 

Etiology

The etiology of Immune Thrombocytopenia (ITP) is not completely understood, and in many cases, the condition is considered idiopathic, meaning that the cause is unknown. However, several factors and conditions have been associated with the development of ITP.  

• Immune System Dysfunction: ITP is primarily considered an autoimmune disorder where the immune system mistakenly attacks and destroys its platelets. The exact trigger for this immune dysregulation is not well-defined, but it is thought to involve a breakdown in immune tolerance. 
• Anti-Platelet Antibodies:  The production of antibodies against platelets, particularly anti-glycoprotein IIb/IIIa and anti-glycoprotein Ib/IX antibodies, is a characteristic feature of ITP. These antibodies target platelets for destruction by the immune system. 
• Viral Infections: In some cases, ITP has been associated with viral infections, especially in children. Certain viruses, such as Epstein-Barr virus, cytomegalovirus, and others, may trigger an immune response that leads to the development of ITP. 
• Chronic Immune Disorders: Individuals with chronic immune disorders, such as systemic lupus erythematosus (SLE) or rheumatoid arthritis, may have an increased risk of developing ITP. 
• Medications: Certain medications have been linked to the development of ITP. Drugs that can induce an immune response or affect platelet function may contribute to the disorder. Examples include heparin, quinine, and some antibiotics. 
• Helicobacter pylori Infection: Some studies suggest an association between Helicobacter pylori (a bacterium that infects the stomach lining) and the development of ITP. Treating H. pylori infection may lead to improvement in some cases of ITP. 
• Genetic Predisposition: While most cases of ITP are sporadic, there may be a genetic predisposition in some individuals. Certain genetic factors could contribute to an increased susceptibility to developing the disorder. 

Genetics

Prognostic Factors

• Platelet Count: The initial platelet count at the time of diagnosis is an important prognostic factor. Individuals with a higher platelet count (above 30,000 to 50,000/microliter) at diagnosis may have a better prognosis compared to those with very low platelet counts. 
• Duration of ITP: The duration of ITP is a significant factor. Acute ITP, especially in children, often resolves spontaneously within a few weeks to months without specific treatment. Chronic ITP, defined as lasting for more than 12 months, may require ongoing management. 
• Age: The age at the time of diagnosis can influence the prognosis. Pediatric ITP often has a more favorable outcome compared to adult-onset ITP. 
• Presence of Bleeding Symptoms: The severity of bleeding symptoms, such as petechiae, bruising, or mucosal bleeding, can impact the prognosis. Individuals with mild or no bleeding symptoms may have a better prognosis than those with severe bleeding. 
• Response to Treatment: The response to initial treatments, such as corticosteroids, intravenous immunoglobulin (IVIG), or other therapies, can provide valuable information about the prognosis. A good response to treatment may suggest a more favorable outcome. 
• Splenectomy: Splenectomy (surgical removal of the spleen) is a treatment option for ITP, particularly in cases that do not respond to other therapies. The decision to undergo splenectomy and the subsequent response to the procedure can impact the long-term prognosis. 
• Underlying Conditions: The presence of underlying conditions, such as autoimmune disorders or infections, can influence the prognosis. Treating the underlying cause, if identified, may improve outcomes. 
• Relapse: Individuals who experience relapses of ITP after an initial response to treatment may have a more challenging prognosis. The frequency and severity of relapses can vary. 

Clinical History

The clinical presentation of Immune Thrombocytopenia (ITP) can vary based on age, associated comorbidities, and the acuity of presentation.  

Pediatric ITP: 

Age Group: Pediatric ITP often occurs in children aged 2 to 10 years. 

Clinical Presentation: 

• Sudden Onset: The onset is often abrupt. 
• Petechiae and Bruising: Common manifestations include petechiae (small red or purple spots on the skin) and easy bruising. 
• Mucosal Bleeding: Some children may experience bleeding from the nose or gums. 
• Asymptomatic: In some cases, children may be asymptomatic, and the diagnosis is made incidentally during a routine checkup. 

Acuity: 

• Self-Limiting: Pediatric ITP is often acute and self-limiting, with a favorable prognosis in many cases. 
• Spontaneous Resolution: Spontaneous resolution without specific treatment is common. 

Adult ITP: 

Age Group: ITP can occur at any age, but it is more commonly diagnosed in adults, particularly those under 40 years old. 

Clinical Presentation: 

• Gradual Onset: The onset may be more gradual compared to pediatric cases. 
• Symptoms of Bleeding: Similar to pediatric cases, adults may experience petechiae, bruising, and mucosal bleeding. 
• Fatigue: Some adults may report fatigue due to lower platelet counts. 

Physical Examination

Skin Examination: 

• Petechiae: Look for small, red, or purple spots on the skin caused by small hemorrhages. Petechiae are a common manifestation of low platelet counts in ITP. 
• Ecchymosis and Bruising: Assess for larger areas of bruising or ecchymosis, which may be more evident in areas prone to trauma. 

Mucous Membranes: 

• Gingival Bleeding: Check for bleeding from the gums, which may indicate a low platelet count. 
• Nasal Bleeding: Assess for epistaxis (nosebleeds), another potential sign of bleeding tendency. 

Lymph Nodes: 

• Palpate Lymph Nodes: Examine for the presence of enlarged lymph nodes, which could suggest an underlying infection or other pathology contributing to ITP. 

Spleen and Liver Examination: 

• Palpate the Spleen and Liver: Enlargement of the spleen or liver may be associated with certain underlying conditions or complications of ITP. 

Neurological Examination: 

• Headache: Assess for headaches, which could be a symptom of increased intracranial pressure in severe cases. 
• Neurological Deficits: In rare cases, severe bleeding in the brain may lead to neurological deficits. A neurological examination can help assess for any signs of intracranial bleeding. 

Blood Pressure Measurement: 

• Blood Pressure Monitoring: In severe cases of ITP, bleeding can lead to a drop in blood pressure. Regular blood pressure monitoring is essential. 

Other Signs of Bleeding: 

• Hematuria: Inquire about or look for signs of blood in the urine, which may indicate bleeding in the genitourinary tract. 
• Gastrointestinal Bleeding: Ask about or look for signs of gastrointestinal bleeding, such as black, tarry stools. 

Musculoskeletal Examination: 

• Joint Pain: In some cases, patients with ITP may experience joint pain, although this is less common than in other forms of arthritis. 

Age group

Associated comorbidity

• Autoimmune Disorders: Adults with ITP may have concurrent autoimmune disorders, such as systemic lupus erythematosus (SLE) or rheumatoid arthritis. 

Acuity: 

• Variable Course: The course of adult ITP can be variable, with some cases becoming chronic. 
• Treatment Considerations: Adults may require ongoing management, and treatment options depend on the severity of symptoms and other factors. 

ITP with Associated Comorbidities: 

• Autoimmune Disorders: ITP may occur in individuals with existing autoimmune conditions, contributing to a more complex clinical picture. 
• Infections: Viral infections, such as Epstein-Barr virus or Helicobacter pylori, may be associated with the development of ITP in some cases. 
• Medication-Induced ITP: Some medications, like heparin or certain antibiotics, may induce an immune response leading to ITP. 

Associated activity

Acuity of presentation

• Acute Presentation: ITP can present acutely with a sudden drop in platelet count and the development of bleeding symptoms. 
• Chronic Presentation: Some cases of ITP have a chronic course, with persistent or recurring low platelet counts over an extended period. 
• Relapsing-Remitting Course: ITP may have a relapsing-remitting course, with periods of low platelet counts and bleeding symptoms followed by periods of remission. 
• Severity of Bleeding: The acuity of presentation may be influenced by the severity of bleeding symptoms, ranging from mild bruising to more serious mucosal or internal bleeding. 

Differential Diagnoses

Secondary Thrombocytopenia: Other underlying medical conditions can lead to a decreased platelet count. Examples include: 

• Infections: Viral (e.g., HIV, hepatitis C), bacterial, or parasitic infections can cause thrombocytopenia. 
• Autoimmune Diseases: Systemic lupus erythematosus (SLE), rheumatoid arthritis, and other autoimmune disorders may be associated with thrombocytopenia. 
• Hematologic Disorders: Aplastic anemia, myelodysplastic syndromes, and leukemia can affect platelet production. 
• Drug-Induced Thrombocytopenia: Certain medications can lead to a drop in platelet count. Examples include heparin, quinine, and some antibiotics. 
• Disseminated Intravascular Coagulation (DIC): DIC is a condition characterized by widespread activation of the clotting cascade, leading to both bleeding and clotting. It can result in a decreased platelet count. 
• Hypersplenism: Enlargement of the spleen (splenomegaly) due to various causes, such as cirrhosis or certain blood disorders, can sequester platelets and cause thrombocytopenia. 
• Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic Uremic Syndrome (HUS): TTP and HUS are rare disorders characterized by microvascular thrombosis and can cause thrombocytopenia. These conditions often present with other features, including hemolytic anemia and organ dysfunction. 
• Congenital Thrombocytopenias: Inherited conditions affecting platelet production or function may present with thrombocytopenia. 
• Pseudothrombocytopenia: This is a laboratory artifact where platelets clump together in a blood sample, giving a falsely low platelet count. Confirmatory testing may be required. 
• Bone Marrow Disorders: Disorders affecting the bone marrow, such as myelofibrosis or infiltration by tumors, can lead to decreased platelet production. 
• Liver Disease: Severe liver disease can impact platelet production and lead to thrombocytopenia. 
• Pregnancy-Related Thrombocytopenia: Gestational thrombocytopenia is a benign condition that can occur during pregnancy and is not associated with bleeding symptoms. It is important to distinguish it from ITP. 

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

The treatment of Immune Thrombocytopenia (ITP) is often individualized based on the patient’s clinical presentation, platelet count, bleeding symptoms, and overall health. The goal of treatment is to raise the platelet count to a level that reduces the risk of bleeding and improves the patient’s quality of life. 

• Observation and Monitoring: In cases of mild ITP with no or minimal bleeding symptoms and a platelet count above a certain threshold, a “watch and wait” approach may be appropriate. Regular monitoring of platelet counts, and clinical symptoms is essential. 
• Corticosteroids: Corticosteroids, such as prednisone or dexamethasone, are often used as a first-line treatment to suppress the immune response and increase platelet counts. They are effective in achieving a rapid response, but long-term use is generally avoided due to the risk of side effects. 
• Intravenous Immunoglobulin (IVIG): IVIG is a treatment option that involves the infusion of immunoglobulins derived from pooled human plasma. It can provide a rapid but temporary increase in platelet counts and is often used in acute situations or prior to surgery. 
• Anti-D Immunoglobulin (Rho(D) Immune Globulin): Anti-D immunoglobulin (e.g., Rhophylac) is used in Rh-positive individuals and can be effective in raising platelet counts. It is typically avoided in Rh-negative individuals and pregnant women. 
• Thrombopoietin Receptor Agonists (TPO-RA): TPO-RAs, such as eltrombopag and romiplostim, stimulate the production of platelets in the bone marrow. They are often considered in cases where other treatments have failed or when a more sustained platelet response is needed. 
• Splenectomy: Surgical removal of the spleen (splenectomy) may be considered in cases of chronic ITP that do not respond to other treatments. Splenectomy can lead to an improvement in platelet counts, but the decision must carefully weigh the potential benefits against the risks of infection. 
• Immunosuppressive Drugs: Immunosuppressive medications, such as azathioprine, mycophenolate mofetil, or cyclosporine, may be used in certain cases to modulate the immune response. 
• Rituximab: Rituximab, a monoclonal antibody, can be considered in refractory cases. It targets B cells, which play a role in the immune response against platelets. 
• Combination Therapy: Some cases may require combination therapy, such as using a TPO-RA along with other medications. 
• Supportive Care: Supportive measures, including the use of antifibrinolytic agents or platelet transfusions in severe bleeding episodes, may be necessary. 

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

use-of-a-non-pharmacological-approach-for-treating-immune-thrombocytopenia

Lifestyle Modifications: 

• Activity Modification: Patients with ITP may be advised to avoid activities that carry a higher risk of injury or bleeding, especially those that may result in trauma or bruising. 

Dietary Considerations: 

• Balanced Diet: Maintaining a well-balanced diet with adequate nutrients, including iron and vitamins, can support overall health. 
• Avoidance of Certain Foods: Some patients may be advised to avoid foods or supplements that may interfere with platelet function or increase the risk of bleeding. 

Stress Management: 

• Mind-Body Techniques: Stress management techniques, such as meditation, mindfulness, and yoga, may be beneficial for reducing stress and promoting overall mental well-being. 
• Counseling or Support Groups: Dealing with a chronic condition like ITP can be emotionally challenging. Counseling or participation in support groups can provide emotional support and coping strategies. 

Physical Therapy: 

• Exercise Programs: Tailored exercise programs, under the guidance of a physical therapist, can help improve muscle strength and coordination, reducing the risk of falls and injuries. 

Bleeding Precautions: 

• Use of Soft Toothbrushes: Patients may be advised to use soft toothbrushes to minimize the risk of gum bleeding during oral care. 
• Avoidance of Certain Medications: Non-steroidal anti-inflammatory drugs (NSAIDs) and other medications that can increase the risk of bleeding may be avoided. 

Regular Monitoring: 

• Platelet Count Monitoring: Regular monitoring of platelet counts is essential to detect changes and assess the need for adjustments in the treatment plan. 

Role of Corticosteroids in the treatment of Immune Thrombocytopenia

Corticosteroids play a significant role in the treatment of Immune Thrombocytopenia (ITP). They are often used as a first-line therapy to rapidly increase platelet counts and manage symptoms associated with low platelets.

The primary goal of corticosteroid treatment in ITP is to suppress the immune system’s attack on platelets, ultimately reducing platelet destruction and increasing their circulation in the bloodstream.

Corticosteroids, such as prednisone or dexamethasone, have potent immunosuppressive effects. They modulate the activity of immune cells, particularly T cells, which are involved in the destruction of platelets. 

Mood changes, increased blood sugar levels, and increased susceptibility to infections. 

Long-term use of corticosteroids is generally limited due to the risk of side effects. In cases of chronic or relapsing ITP, alternative treatments or maintenance therapies may be considered. 

prednisone 

prednisone belongs to the class of corticosteroids, which have potent immunosuppressive effects. These medications work by suppressing the immune system, particularly T cells, to reduce the destruction of platelets.

It is typically administered orally in the form of tablets or liquid. The initial treatment often involves a high dose of prednisone to achieve a quick response and increase platelet counts. This high dose is often referred to as “pulse” or “burst” therapy.

After achieving the desired increase in platelet counts, the dosage of prednisone is gradually tapered over some time. Tapering helps to minimize the risk of side effects associated with prolonged steroid use. 

Role of Intravenous Immunoglobulin (IVIG) in Immune Thrombocytopenia (ITP)

Intravenous Immunoglobulin (IVIG) is a therapeutic option used in the treatment of Immune Thrombocytopenia (ITP). IVIG is a blood product that contains pooled immunoglobulins, which are antibodies derived from the plasma of thousands of healthy donors.

The use of IVIG in ITP is aimed at modulating the immune system and increasing platelet counts. IVIG is administered through intravenous infusion. The duration of the infusion can vary, but it is typically given over a few hours. 

IVIG is often used in acute situations, such as when patients with ITP present with severe bleeding symptoms or very low platelet counts and a need for rapid platelet increase. IVIG may be administered before surgery or other medical procedures to increase platelet counts and reduce the risk of bleeding. 

Anti-D Immunoglobulin (Rho(D) Immune Globulin) for the treatment of Immune Thrombocytopenia

Anti-D Immunoglobulin, also known as Rho(D) Immune Globulin or RhIg, is primarily used for the prevention of Rh(D) alloimmunization in Rh-negative individuals. Rh(D) alloimmunization occurs when an Rh-negative person is exposed to Rh-positive blood, leading to the production of antibodies against Rh-positive red blood cells. This is particularly relevant in pregnancy when an Rh-negative mother carries an Rh-positive fetus. 

Role of Thrombopoietin Receptor Agonists in the treatment of Immune thrombocytopenia

Thrombopoietin Receptor Agonists (TPO-RAs) are a class of medications used in the treatment of Immune Thrombocytopenia (ITP), a condition characterized by low platelet counts due to immune system-mediated destruction of platelets. TPO-RAs work by stimulating the production of platelets in the bone marrow, and they can be effective in increasing platelet counts in patients with ITP.  

Stimulation of Platelet Production: TPO-RAs, such as eltrombopag and romiplostim, mimic the action of thrombopoietin, a natural hormone that regulates platelet production. By binding to the thrombopoietin receptor (c-Mpl) on megakaryocytes in the bone marrow, TPO-RAs stimulate the production and maturation of platelets. 

Bone Marrow Response: TPO-RAs act on the bone marrow to increase the number and size of megakaryocytes, leading to enhanced platelet production and release into the bloodstream. 

• eltrombopag: Oral TPO-RA is taken once daily. It is approved for the treatment of chronic ITP in adults and children. 
• romiplostim: It is administered as a subcutaneous injection. It is typically given once weekly and is approved for adults with chronic ITP who have had an insufficient response to other treatments. 

Use of CD20 Inhibitor (Monoclonal antibody) in Immune Thrombocytopenia (ITP): Exploring Efficacy and Considerations in Second-Line Therapy

rituximab 

rituximab is indeed typically considered in second-line therapy for immune thrombocytopenia (ITP), especially when initial treatments have not been effective or in cases of chronic or refractory ITP.  

rituximab is often used as a second-line treatment in ITP when other treatments have not been effective. It has a response rate of over 50%, indicating its efficacy in some patients with ITP.

Prior to rituximab use, a hepatitis panel is checked to assess the risk of Hepatitis B reactivation. There is a small risk of PML, a rare and serious brain infection. 

rituximab administration may impact the timing of COVID vaccinations, with a recommended delay of 6 to 12 months. 

There is a possible 20% risk of hypogammaglobulinemia when rituximab is coadministered with dexamethasone, necessitating intravenous immunoglobulin (IV-IgG) replacement. 

use-of-intervention-with-a-procedure-in-treating-immune-thrombocytopenia

The primary treatments for Immune Thrombocytopenia (ITP) typically involve medications aimed at modulating the immune system or stimulating platelet production.

However, in specific situations, interventions with procedures may be considered, especially when there’s a need for rapid control of bleeding or in cases of severe thrombocytopenia. Some interventions that might be considered include: 

• Platelet Transfusion: Platelet transfusions may be administered in emergencies or when there is severe bleeding. However, it’s important to note that platelet transfusions provide only a temporary increase in platelet counts and are not a long-term solution. 
• Splenectomy: Surgical removal of the spleen (splenectomy) is a treatment option for ITP, especially in cases where other treatments have failed or are not well-tolerated. The spleen is a site where platelets are sequestered and destroyed in ITP. Removing the spleen can reduce platelet destruction and increase platelet counts. However, splenectomy is generally reserved for cases of chronic or refractory ITP due to potential long-term risks and complications. 
• Rituximab and plasmapheresis: While rituximab is primarily a medication, it can be administered via infusion. Plasmapheresis is a procedure that involves removing, treating, and then returning blood plasma to the body. These interventions might be considered in specific cases, but they are not typical procedural interventions. 

use-of-phases-in-managing-immune-thrombocytopenia

Observation and Monitoring: 

• Low-risk Cases: In some mild cases, especially in children, observation without immediate intervention may be appropriate. Regular monitoring of platelet counts helps determine if treatment is necessary. 

Acute Phase: 

• Corticosteroids: Prednisone or other corticosteroids are often used initially to suppress the immune response and increase platelet counts quickly. 

Initial Response Assessment: 

• Platelet Count Monitoring: After initiating treatment, it is crucial to monitor platelet counts regularly to assess the patient’s response. 

Second-Line Therapy: 

If corticosteroids alone are not sufficient, second-line therapies may be considered, such as: 

• Intravenous Immunoglobulin (IVIG): Provides a quick but temporary increase in platelet count. 
• Anti-D Immunoglobulin (Rho(D) Immune Globulin): Particularly used in Rh-positive individuals. 
• Thrombopoietin Receptor Agonists (TPO-RAs): Stimulate platelet production. 

Chronic Phase Management: 

• Tapering Steroids: If corticosteroids are used initially, efforts are made to taper the dose to the lowest effective level to minimize side effects. 
• TPO-RAs: Long-term use of thrombopoietin receptor agonists may be considered for chronic ITP to maintain platelet counts. 
• Immunosuppressive Agents: Azathioprine, mycophenolate mofetil, or cyclosporine may be used for those who do not respond well to other treatments. 

Rescue Therapies: 

• Splenectomy: Surgical removal of the spleen may be considered in cases where other treatments have failed, especially in patients who do not respond to medical therapy. 
• Rituximab: A monoclonal antibody that targets B cells, it may be considered in refractory cases. 

Supportive Care: 

• Platelet Transfusions: In emergencies or for patients at risk of bleeding, platelet transfusions may be used to raise platelet counts quickly. 

Patient Education and Psychosocial Support: 

• Educate patients about their condition, treatment options, and potential side effects. 
• Provide psychological support to help cope with the chronic nature of the disease. 

Medication

Future Trends

Media Gallary

References

Immune Thrombocytopeni purpura:.ncbi.nlm.nih