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# Immune thrombocytopenias: ITP and HIT

- Lesion

Antibodies coat platelets so the spleen removes them. Most cases bleed; one drug reaction, heparin-induced, clots instead.

Updated Nov 12, 2026

## Key points

- ITP: isolated thrombocytopenia, large platelets, normal or increased megakaryocytes, normal spleen size; a diagnosis of exclusion.
- The spleen is both the main site of platelet removal and a source of autoantibodies.
- Acute ITP: children one to two weeks after a viral illness; usually resolves within six months.
- HIT type II: five to fourteen days after heparin begins (sooner if recently exposed); antibodies to PF4–heparin; venous and arterial thrombosis.
- In HIT stop all heparin, including low-molecular-weight heparin, and use a non-heparin anticoagulant.

## What it is

Immune thrombocytopenias are caused by antibodies that shorten platelet survival. Chronic immune thrombocytopenic purpura (ITP) is mostly a disease of adult women, with IgG autoantibodies against GPIIb/IIIa or GPIb/IX; it may be primary or secondary to lupus, HIV or CLL. Acute ITP is a self-limited disease of children after a viral infection. Drugs such as quinine, quinidine and vancomycin trigger drug-dependent antibodies. Heparin-induced thrombocytopenia (HIT) is caused by antibodies against heparin–platelet factor 4 complexes that activate platelets and cause thrombosis. HIV infects megakaryocytes and promotes autoantibodies.

## Structure

- Marrow: normal or increased megakaryocytes, some large and immature.
- Spleen: normal size, congested sinusoids, prominent follicles and occasional megakaryocytes in sinuses.
- Skin and mucosa: petechiae, ecchymoses; rarely intracranial bleeding.

## Step by step

- IgG autoantibodies (or drug-dependent antibodies) bind platelet membrane glycoproteins.
- Fc receptors on splenic macrophages recognize opsonized platelets and remove them.
- Antibodies may also injure megakaryocytes, reducing production.
- In HIT, antibodies bind PF4–heparin complexes on platelets and activate them through Fc receptors.
- Activated platelets release procoagulant microparticles: thrombosis despite low counts.

## Immune thrombocytopenias compared

| Type | Who and trigger | Target | Outcome |
| --- | --- | --- | --- |
| [Chronic ITP](https://durgical.com/en/conditions/immune-thrombocytopenia/) | Adult women; primary or with lupus, HIV, CLL | GPIIb/IIIa or GPIb/IX | Chronic, responds to glucocorticoids, splenectomy or other therapy |
| [Acute ITP](https://durgical.com/en/conditions/immune-thrombocytopenia/) | Children after a viral infection | Platelet glycoproteins | Usually resolves within six months |
| Drug-induced | Quinine, quinidine, vancomycin, GPIIb/IIIa inhibitors | Drug-dependent epitopes | Resolves when the drug is stopped |
| [Heparin-induced (type II)](https://durgical.com/en/conditions/heparin-induced-thrombocytopenia/) | Five to fourteen days of heparin | PF4–heparin complexes | Thrombosis, limb loss risk |
| [HIV-associated](https://durgical.com/en/conditions/hiv-infection-and-aids/) | HIV infection | GPIIb/IIIa autoantibodies plus infected megakaryocytes | Improves with antiretroviral therapy |

## Clinical notes

- Easy bruising, nosebleeds and gum bleeding in a woman with no splenomegaly or lymphadenopathy suggests chronic ITP.
- Splenomegaly in apparent ITP points to another cause, such as lymphoma.

## Memory aid

ITP bleeds and the spleen eats; HIT clots and the platelets fire.

## Test yourself

Think of the answer, then tap the question to see it.

## Which platelet glycoproteins are targeted in chronic ITP?

GPIIb/IIIa and GPIb/IX.

## Why does heparin-induced thrombocytopenia cause thrombosis?

Antibodies to PF4–heparin complexes activate platelets, which release procoagulant material.

## Why does splenectomy help in ITP?

The spleen is the main site of removal of antibody-coated platelets and also a source of the autoantibodies.

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## Elsewhere in DurgiPedia

- [Type II hypersensitivity (antibody against cells)](https://durgical.com/en/immunology/type-ii-hypersensitivity/)
- [Primary hemostasis and platelets](https://durgical.com/en/physiology/primary-hemostasis-and-platelets/)

## Connections

## Related 4

- [Hypercoagulable states: inherited and acquired](https://durgical.com/en/general-pathology/hypercoagulable-states-inherited-and-acquired/)
- [Thrombocytopenia: mechanisms](https://durgical.com/en/general-pathology/thrombocytopenia-mechanisms/)
- [Immunohaemolytic anaemia](https://durgical.com/en/general-pathology/immunohaemolytic-anaemia/)
- [Hemorrhage: petechiae, purpura, ecchymosis, hematoma, and what blood loss does](https://durgical.com/en/general-pathology/hemorrhage-petechiae-purpura-ecchymosis-hematoma-and-what-blood-loss-does/)

## Related conditions 5

- [Immune thrombocytopenia (ITP)](https://durgical.com/en/conditions/immune-thrombocytopenia/)
- [Heparin-induced thrombocytopenia](https://durgical.com/en/conditions/heparin-induced-thrombocytopenia/)
- [HIV infection and AIDS](https://durgical.com/en/conditions/hiv-infection-and-aids/)
- [Systemic lupus erythematosus](https://durgical.com/en/conditions/systemic-lupus-erythematosus/)
- [Chronic lymphocytic leukaemia](https://durgical.com/en/conditions/chronic-lymphocytic-leukaemia/)

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Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.

Sources: [Immune thrombocytopenic purpura (ITP): MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000535.htm) (MedlinePlus, US National Library of Medicine, 2026).

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Representative model, for educational purposes only.

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License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/general-pathology/immune-thrombocytopenias-itp-and-hit/