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Immune Thrombocytopenia (ITP)

High EvidenceUpdated: 2025-12-23

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Red Flags

  • Wet Purpura (mucosal bleeding - e.g., blood blisters in mouth) -> High risk of Intracranial Haemorrhage
  • Severe Headache (Exclude ICH)
  • Fever + Confusion + Fragmented cells (Consider TTP - Thrombotic Thrombocytopenic Purpura)
Overview

Immune Thrombocytopenia (ITP)

[!WARNING] Medical Disclaimer: This content is for educational and informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional for diagnosis and treatment. Medical guidelines and best practices change rapidly; users should verify information with current local protocols.

1. Overview

Immune Thrombocytopenia (ITP) is an autoimmune disorder characterised by isolated thrombocytopenia and mucocutaneous bleeding.

Historically called "Idiopathic Thrombocytopenic Purpura", the name has changed:

  • Immune: We know the cause is autoimmune.
  • Thrombocytopenia: Platelets are low.
  • (Purpura is often absent).

Classification

  • Newly Diagnosed: < 3 months.
  • Persistent: 3–12 months.
  • Chronic: > 12 months.

Clinical Scenario: The Bruised Gymnast

A 25-year-old female presents with unexplained bruising on her legs and prolonged nosebleeds. She is otherwise fit and well. FBC shows Platelets 8 x 10^9/L. Hb and WCC are normal. Examination is unremarkable (no splenomegaly).

Key Teaching Points

  • This is the classic presentation of ITP: An isolated severe thrombocytopenia in a well patient.
  • The absence of splenomegaly is crucial (if spleen is big, think Lymphoma/Leukaemia/Hypersplenism).
  • Peripheral Blood Film must be requested to rule out pseudothrombocytopenia (clumping) and TTP (fragments).
  • Admission is required due to bleeding risk (&lt;20).
2. Epidemiology
  • Children: Usually acute, following a viral infection. Self-limiting.
  • Adults: Usually chronic.
  • Sex: Female > Male (2:1 in young adults).
  • Incidence: 3 per 100,000 per year.
3. Pathophysiology
  1. Destruction: IgG autoantibodies target platelet surface antigens (GPIIb/IIIa or GPIb/IX).
  2. Clearance: Antibody-coated platelets are recognised by Fc receptors on Macrophages in the Spleen (and Liver) and destroyed.
  3. Impaired Production: Antibodies also attack Megakaryocytes in the bone marrow, reducing platelet production (inhibiting TPO effect).
4. Clinical Presentation

Important Negative: There should be NO splenomegaly in primary ITP.

Asymptomatic
Incidental finding on bloods.
Cutaneous Bleeding
Petechiae: Pinpoint non-blanching red spots (usually dependent areas). Purpura: Larger purple spots. Ecchymoses: Easy bruising.
Mucosal Bleeding ("Wet Purpura")
Epistaxis. Gingival bleeding. Menorrhagia. Blood blisters in mouth (Bullous haemorrhagic angina) - Red Flag for ICH risk.
Severe
Intracranial Haemorrhage (ICH) or GI bleed (<1%).
5. Clinical Examination
  1. Skin: Assess extent of purpura/bruising.
  2. Mouth: Check for "wet" bleeding.
  3. Abdomen: Palpate for spleen (if palpable, question the diagnosis).
  4. Lymph Nodes: Should be normal.
6. Investigations

ITP is a diagnosis of exclusion.

First Line

  • FBC: Isolated thrombocytopenia. Hb and WCC normal.
  • Blood Film: Confirm true low platelets. Look for large/giant forms (young platelets). Exclude Schistocytes (fragments -> TTP). Exclude Blasts (Leukaemia).
  • Coagulation Screen: Normal in ITP. (Deranged in DIC).
  • Viral Screen: HIV, Hep B, Hep C (mandatory).
  • Autoimmune: ANA (can be secondary to SLE).

Second Line

  • Bone Marrow Biopsy:
    • Not routine, especially in typical cases <60 years.
    • Shows increased megakaryocytes.
7. Management

Goal: Prevent serious bleeding, not to normalise count.

Indication for Treatment

  • Count > 30 and no bleeding: Observe.
  • Count < 30 or significant bleeding: Treat.

First Line (Emergency/Initial)

  1. Corticosteroids:
    • Prednisolone (1 mg/kg for 2-4 weeks then taper). Or Dexamethasone (40mg pulse for 4 days).
    • Stops macrophage destruction.
  2. IVIg (Intravenous Immunoglobulin):
    • For rapid rise (e.g., pre-op or active bleed).
    • Mechanism: Overwhelms/blocks Fc receptors on macrophages ("distracting them"). Effect lasts 2-4 weeks.
  3. Platelet Transfusion:
    • Generally useless (consumed in minutes).
    • Only used in life-threatening haemorrhage alongside IVIg/Steroids.

Second Line (Persistent/Chronic)

If steroids fail or dependence develops:

  1. TPO Receptor Agonists (TPO-RAs):
    • Eltrombopag (Oral), Romiplostim (SC injection).
    • Stimulate marrow production. highly effective.
  2. Rituximab:
    • Anti-CD20 monoclonal antibody. Depletes B cells (antibody factories).
  3. Splenectomy:
    • Removes the site of destruction.
    • Permanent cure in 60-70%.
    • Relegated to 3rd line due to infection risk and success of medical therapy.
8. Complications
  • Hemorrhage: ICH is the main cause of death (risk increases with age >60 and count <10).
  • Treatment Side Effects:
    • Steroids: Diabetes, Hypertension, Osteoporosis, Cushings.
    • Splenectomy: Sepsis (OPSI).
9. Prognosis & Outcomes
  • Children: >80% spontaneously remit within 6-12 months.
  • Adults: Only 10-20% spontaneously remit. Most require monitoring or chronic treatment.
10. Evidence & Guidelines
  • ASH (American Society of Hematology) Guidelines 2019.
  • International Consensus Report 2019: Shifted towards TPO-RAs earlier to avoid long-term steroid toxicity.
11. Patient & Layperson Explanation

What is ITP? It is a condition where your immune system gets confused and attacks your own platelets.

  • Platelets are the tiny cells that help blood clot.
  • When they are low, you bruise easily or bleed.

Why did I get it? In adults, we often don't know (idiopathic). In children, it often happens after a virus. It is not a cancer.

Is it dangerous? If the platelet count drops very low (single digits), there is a risk of spontaneous serious bleeding, like a brain bleed. However, most people have "safe" low levels (above 30) where normal life is fine.

How do we treat it? If your count is safe and you aren't bleeding, we just watch you. If we need to raise the count, we use:

  1. Steroids: To calm the immune system.
  2. Injections (IVIg): To quickly block the destruction.
  3. Bone Marrow Boosters: Drugs that tell your body to make more platelets.
  4. Surgery: Removing the spleen (which is where the platelets are being destroyed) is a last resort.
12. References
  1. Provan D, et al. Updated international consensus report on the investigation and management of primary immune thrombocytopenia. Blood Adv. 2019;3(22):3780-3817.
  2. Neunert C, et al. American Society of Hematology 2019 guidelines for immune thrombocytopenia. Blood Adv. 2019;3(23):3829-3866.
  3. Cooper N, Ghanima W. Immune Thrombocytopenia. N Engl J Med. 2019;381:945-955.

Last updated: 2025-12-23

At a Glance

EvidenceHigh
Last Updated2025-12-23

Red Flags

  • Wet Purpura (mucosal bleeding - e.g., blood blisters in mouth) -> High risk of Intracranial Haemorrhage
  • Severe Headache (Exclude ICH)
  • Fever + Confusion + Fragmented cells (Consider TTP - Thrombotic Thrombocytopenic Purpura)

Clinical Pearls

  • Male (2:1 in young adults).
  • TTP). Exclude Blasts (Leukaemia).

Guidelines

  • NICE Guidelines
  • BTS Guidelines
  • RCUK Guidelines